Sugar Cravings

Why do people get sugar cravings? I have discovered that sugar is addictive.

I try to eat less than the daily recommended amount of sugar, by not purchasing sugary products. My CLIF Builder bars have 23g each, so I limit myself to eating only one bar per day.

Sugar Cravings

I recently went to an event that included lunch and some desserts. I took one small brownie square with my meal. Afterwards, I went back for another brownie square. And then another brownie square. These were not normal brownies. They kind of looked like brownies, but they were caked in sugar.

I got sugar cravings after eating just one of these brownies!

Sugar Cravings Causes

Evidence reveals sugar can be addictive. Experts say moderation is not the best option — elimination is.

Good brownies contain minimal salt and almost no sugar.

Eating sugar and processed foods creates a vicious cycle spurred on by addiction.  Even a diet of sugar from high fructose corn syrup will promote a sugar addition.

High fructose corn syrup also promotes a number of other maladies, including:

So sugar cravings are caused by eating sugary foods and drinks, foods you crave, adrenal fatigue, monthly hormonal changes in women, parasites, Candida, and bacterial overgrowth.

 

Dr. Mercola and Gary Taubes on The Case Against Sugar Video

Gary Taubes:

It’s also known that sugar induces similar responses in the “reward centers” of the human brain as other additive substances, like nicotine, cocaine, heroin and alcohol. The 12-step Alcoholics Anonymous program even recommends consuming sweets in lieu of alcohol to ward off a craving for a drink.

Today, “Sugar has become an ingredient in prepared and packaged foods so ubiquitous it can only be avoided by concerted and determined effort,” Taubes wrote, which is, of course, precisely the problem, especially as realization grows that simply “moderating” sugar may not be enough. Taubes continued:17

“The traditional response to the how-little-is-too-much question is that we should eat sugar in moderation — not eat too much of it. But we only know we’re consuming too much when we’re getting fatter or manifesting other symptoms of insulin resistance and metabolic syndrome … Any discussion of how little sugar is too much also has to account for the possibility that sugar is a drug and perhaps addictive.

Trying to consume sugar in moderation, however it’s defined, in a world in which substantial sugar consumption is the norm and virtually unavoidable, is likely to be no more successful for some of us than trying to smoke cigarettes in moderation — just a few a day, rather than a whole pack … If sugar consumption is a slippery slope, then advocating moderation is not a meaningful concept.”

Big Sugar and Coke Conspiracy

Probiotics Tablets

Probiotics tablets may be taken for a number of conditions, such as:

  • AAD – Antibiotic associated diarrhea – Prevention (II)
    C – Constipation (I)🍁
  • CDAD – Clostridium difficile associated diarrhea – Prevention (I)🍁
    HP – Helicobacter pylori – Adjunct to standard eradication therapy (I)
  • IBD-P – Inflammatory bowel disease – Pouchitis (I)🍁
    IBD-UC – IBD – Ulcerative colitis – Adjunct to standard therapy (I)🍁
  • IBS – Irritable bowel syndrome (I)🍁
  • LH – Liver Health (NASH/NAFLD/MHE; as adjunct to standard therapy; see studies for specific population) (I)
    ID – Infectious diarrhea (II)
  • M/A – Mood and Affect (symptoms related to stress/anxiety; not a substitute for standard treatment) (II)
  • TD – Traveler’s diarrhea prevention (I)
  • OH – Oral health (reductions of tonsillitis, laryngitis, and dental caries) (II)🍁
  • WM – Weight Management (aids in reduction of body weight, body fat mass and waist circumference) (I)🍁

Probiotics Tablets for H.Pylori:

Showing 1 to 8 of 8 entries

Probiotic Chart Source: http://www.probioticchart.ca/PBCAdultHealth.html?utm_source=adult_ind&utm_medium=civ&utm_campaign=CDN_CHART

 

http://www.probioticchart.ca/PBCAdultHealth.html?utm_source=adult_ind&utm_medium=civ&utm_campaign=CDN_CHART

Top 3 Apples to Eat

The top 3 apples to eat that also provide the highest in overall nutrients are:

  1. Fuji (bright, juicy and crisp)
  2. Gala (mild and pleasant)
  3. Jonagold (traditional, sweet and tart)

The Least Appealing Apples

  • Granny Smith (green and tart)
  • Red Delicious (sweet and classic)
  • Reineta (mottled green, from Spain)

No apple is a bad apple. But these 3 apples are at the bottom of the barrel for overall nutrients.

  • Empire (crunchy and sweet)
  • Cortland (tart and crisp)
  • Golden Delicious (sweet and delicate)

Apple phytochemicals and their health benefits

Abstract

Evidence suggests that a diet high in fruits and vegetables may decrease the risk of chronic diseases, such as cardiovascular disease and cancer, and phytochemicals including phenolics, flavonoids and carotenoids from fruits and vegetables may play a key role in reducing chronic disease risk. Apples are a widely consumed, rich source of phytochemicals, and epidemiological studies have linked the consumption of apples with reduced risk of some cancers, cardiovascular disease, asthma, and diabetes. In the laboratory, apples have been found to have very strong antioxidant activity, inhibit cancer cell proliferation, decrease lipid oxidation, and lower cholesterol. Apples contain a variety of phytochemicals, including quercetin, catechin, phloridzin and chlorogenic acid, all of which are strong antioxidants. The phytochemical composition of apples varies greatly between different varieties of apples, and there are also small changes in phytochemicals during the maturation and ripening of the fruit. Storage has little to no effect on apple phytochemicals, but processing can greatly affect apple phytochemicals. While extensive research exists, a literature review of the health benefits of apples and their phytochemicals has not been compiled to summarize this work. The purpose of this paper is to review the most recent literature regarding the health benefits of apples and their phytochemicals, phytochemical bioavailability and antioxidant behavior, and the effects of variety, ripening, storage and processing on apple phytochemicals.

Keywords: apples, antioxidants, phytochemicals, cancer, cardiovascular disease, phenolics, flavonoids, fruit

Background

In the United States, as well as in most industrialized countries, cardiovascular disease and cancer are ranked as the top two leading causes of death. The causes of both diseases have been linked to lifestyle choices, and one of the most important is diet. It has been estimated that a healthy diet could prevent approximately 30% of all cancers [,]. High cholesterol and obesity are greatly influenced by diet and lifestyle and are costing the United States billions of dollars in health related expenses. High cholesterol, a risk factor for cardiovascular disease, is commonly treated with statin drugs, and it has been estimated that the United States will spend 30 billion dollars per year on cholesterol treatment by statin drugs []. In 1998, obesity, a risk factor for cardiovascular disease, cancer, and diabetes, has been estimated to cost the United States over 92 billion dollars per year []. Understanding the effects of diet on chronic disease may greatly aid in the prevention of chronic disease.

As children, many of us were told to “eat your vegetables because they are good for you”, and the adage “an apple a day keeps the doctor away” is still quite popular. Recently, many studies have provided the scientific backing for both of these very common phrases. In the early 1990’s, researchers examined well over one hundred epidemiological studies relating to diet and cancer, and in 128 of 156 dietary studies, fruits and vegetables had a significant protective effect against a variety of different cancers []. They found that those who consumed low amounts of fruits and vegetables were twice as likely to have cancer compared to those who ate high amounts of fruits and vegetables. Recently, a study linked intake of fruits and vegetables with a reduced risk in breast cancer in woman in China []. In this population based, case-control study of women in Shanghai, pre-menopausal women who ate more dark yellow-orange vegetables and more citrus fruits tended to have lower breast cancer risk. Fruit and vegetable intake also appears to have a protective effect against coronary heart disease []. Approximately 84,000 women were followed for 14 years and 42,000 men were followed for 8 years. They found that people who ate the highest amount of fruits and vegetables had a 20% lower risk for coronary heart disease, and the lowest risks were seen in people who consumed more green leafy vegetables, and fruits rich in vitamin C. Not only may a diet high in fruits and vegetables help prevent heart disease and cancer, but it may also help protect against a variety of other illnesses. For example, a diet high in fruits and vegetables may help protect against cataracts, diabetes, Alzheimer disease, and even asthma [].

Much of the protective effect of fruits and vegetables has been attributed to phytochemicals, which are the non-nutrient plant compounds such as the carotenoids, flavonoids, isoflavonoids, and phenolic acids. Thousands of phytochemicals have been identified in foods, yet there are still many that have not been identified. Different phytochemicals have been found to possess a range of activities, which may help in protecting against chronic disease. For example, phytochemicals may inhibit cancer cell proliferation, regulate inflammatory and immune response, and protect against lipid oxidation [,]. A major role of the phytochemicals is protection against oxidation. We live in a highly oxidative environment, and many processes involved in metabolism may result in the production of more oxidants. Humans, and all animals, have complex antioxidant defense systems, but they are not perfect and oxidative damage will occur. Both cardiovascular disease and cancer are thought to be particularly the results of oxidative stress, which can lead to damage of the larger biomolecules, such as DNA, lipids, and proteins. It has been estimated that there are 10,000 oxidative hits to DNA per cell per day in humans [].

A major class of phytochemicals found commonly in fruits and vegetables are the flavonoids. Apples are a very significant source of flavonoids in people’s diet in the US and in Europe. In the United States, twenty-two percent of the phenolics consumed from fruits are from apples making them the largest source of phenolics []. In Finland, apples and onions are main sources of dietary flavonoids, while in the Netherlands apples rank third behind tea and onions as top sources of flavonoids [,]. In a Finnish study of approximately 10,000 people, flavonoid intake was associated with a lower total mortality []. Apples were one of the main sources of dietary flavonoids that showed the strongest associations with decreased mortality.

Not only are apples commonly enjoyed by many cultures, but they are also a good source of antioxidants. When compared to many other commonly consumed fruits in the United States, apples had the second highest level of antioxidant activity (Figure  (Figure1).1). Apples also ranked the second for total concentration of phenolic compounds, and perhaps more importantly, apples had the highest portion of free phenolics when compared to other fruits []. This means that these compounds are not bound to other compounds in the fruits, and the phenolics may be more available for eventual absorption into the bloodstream.

Figure 1

Antioxidant activity of various fruit extracts (mean ± SD, n = 3).

Since fruits and vegetables are high in antioxidants, a diet high in these foods should help prevent oxidative stress, and may therefore help prevent chronic disease and slow aging. These findings have lead to the National Research Council to recommend consuming five or more servings of fruits and vegetables a day. Several commonly consumed foods and beverages, including tea, wine, onions, cocoa, cranberries, and apples, have been targeted as particularly beneficial in the diet because of their high content of phenolic compounds. While active research into the health benefits of these foods has been ongoing, current reviews of this work exist for all of the above-mentioned foods except apples. Therefore, the purpose of this paper is to review the recent literature addressing the health benefits of apples, their phytochemical profile, bioavailability of apple phytochemicals, and factors that may affect the phytochemical quality, such as apple variety, ripening, storage, and processing.

Health benefits of apples: epidemiological evidence

Cancer

Several studies have specifically linked apple consumption with a reduced risk for cancer, especially lung cancer. In the Nurses’ Health Study and the Health Professionals’ Follow-up Study, involving over 77,000 women and 47, 000 men, fruit and vegetable intake was associated with a 21% reduced risk in lung cancer risk in women, but this association was not seen in men []. Very few of the individual fruits and vegetables examined had a significant effect on lung cancer risk in women, however apples were one of the individual fruits associated with a decreased risk in lung cancer. Women who consumed at least one serving per day of apples and pears had a reduced risk of lung cancer []. Of the men involved, there was no association seen between any individual fruit or vegetable and lung cancer risk.

In a case control study in Hawaii, it was found that apple and onion intake was associated with a reduced risk of lung cancer in both males and females []. Smoking history and food intake was assessed for 582 patients with lung cancer and 582 control subjects without lung cancer. There was a 40–50% decreased risk in lung cancer in participants with the highest intake of apples, onions, and white grapefruit when compared to those who consumed the lowest amount of these fruits. The decreased risk in lung cancer was seen in both men and women and in almost all ethnic groups. No associations were seen with red wine, black tea or green tea. Both onions and apples are high in flavonoids, especially quercetin and quercetin conjugates []. Le Marchand et al. [] found an inverse association between lung cancer and quercetin intake although the trend was not statistically significant. Interestingly, the inverse association seen between apple and onion intake and lung cancer were stronger for squamous cell carcinomas than for adenocarcinomas.

In a Finnish study involving 10,000 men and women and a 24-year follow-up, a strong inverse association was seen between flavonoid intake and lung cancer development []. In the sampled population, the mean flavonoid intake was 4.0 mg per day, and 95% of the total flavonoid intake was quercetin. Apples and onions together provided 64% of all flavonoid intake. The reduced risk of lung cancer associated with increased flavonoid consumption was especially strong in younger people and in nonsmokers. Apples were the only specific foods that were inversely related to lung cancer risk. Since apples were the main source of flavonoids in the Finnish population, it was concluded that the flavonoids from apples were most likely responsible for the decreased risk in lung cancer.

The relationship of dietary catechins and epithelial cancer was examined in 728 men (aged 65–84) as part of the Zutphen Elderly Study []. Tea, a naturally high source of catechins, contributed 87% of the total catechin intake in this study, while apples contributed 8.0% of catechin consumption. It was found that total catechin and tea consumption did not have an effect on lung cancer, but apple consumption was associated with decreased epithelial lung cancer incidence []. This supported the findings of the previous studies discussed, where apples were significantly inversely associated with lung cancer, and may suggest that catechins alone do not play have a effect against lung cancers. Other data from the Zutphen Elderly study showed an inverse association between fruit and vegetable flavonoids and total cancer incidence and tumors of the alimentary and respiratory tract []. Again, tea flavonoids were not associated with a decrease in cancer risk.

Cardiovascular disease

A reduced risk of cardiovascular disease has been associated with apple consumption. The Women’s Health Study surveyed nearly 40,000 women with a 6.9-year follow-up, and examined the association between flavonoids and cardiovascular disease []. Women ingesting the highest amounts of flavonoids had a 35% reduction in risk of cardiovascular events. Flavonoid intake was not associated with risk of stroke, myocardial infarction, or cardiovascular disease death. Quercetin did not have any association with cardiovascular disease, cardiovascular events, myocardial infarction or stroke. However, both apple intake and broccoli intake were associated with reductions in the risk of both cardiovascular disease and cardiovascular events. Women ingesting apples had a 13–22% decrease in cardiovascular disease risk.

In a Finnish study examining flavonoid intake and coronary mortality, it was found that total flavonoid intake was significantly inversely associated with coronary mortality in women, but not in men []. Apple and onion intake was also inversely associated with coronary mortality, especially in women. Data collected from this same cohort study also showed the effect of quercetin and apple intake on cerebrovascular disease []. Those who had the highest consumption of apples had a lower risk of thrombotic stroke compared to those who consumed the lowest amounts of apples []. Onion intake and quercetin intake were not associated with thrombotic stroke or other cerebrovascular diseases.

Apple and wine consumption was also inversely associated with death from coronary heart disease in postmenopausal women in a study of nearly 35,000 women in Iowa []. The intakes of catechin and epicatechin, both constituents of apples, were strongly inversely associated with coronary heart disease death. Although total catechin intake was inversely associated with coronary heart disease mortality, Arts et al (2001) found that tea catechins were not associated with coronary heart disease mortality in postmenopausal women. Apple catechins may be more bioavailable than the catechin and epicatechin gallates commonly found in teas.

The relationship between flavonoids and risk of coronary heart disease were also examined as part of the Zutphen Elderly Study []. Flavonoid intake was strongly correlated with a decreased mortality from heart disease in elderly men and also negatively correlated with myocardial infarction. Tea was the main source of flavonoids in this study and was also negatively correlated with coronary heart disease. Apple intake contributed to approximately 10% of the total ingested flavonoids and was also associated with a reduced risk of death from coronary heart disease in men, however the relationship was not statistically significant [].

Asthma and pulmonary function

Apple consumption has been inversely linked with asthma and has also been positively associated with general pulmonary health. In a recent study involving 1600 adults in Australia, apple and pear intake was associated with a decreased risk of asthma and a decrease in bronchial hypersensitivity, but total fruit and vegetable intake was not associated with asthma risk or severity []. Specific antioxidants, such as vitamin E, vitamin C, retinol, and β-carotene, were not associated with asthma or bronchial hypersensitivity. Previously it had been found that apple intake, as well as selenium intake, was associated with less asthma in adults in the United Kingdom []. This study surveyed nearly 600 individuals with asthma and 900 individuals without asthma about their diet and lifestyle. Total fruit and vegetable intake was weakly associated with asthma, and apple intake showed a stronger inverse relationship with asthma. This latter effect was most clear in subjects who consumed at least two apples per week. Onion, tea, and red wine consumption were not related to asthma incidence, suggesting an especially beneficial effect of apple flavonoids. Vitamin C and vitamin E were not correlated with asthma incidence, and carotene intake was weakly, but positively, associated with asthma. Apple intake and orange intake were both associated with a reduced incidence of asthma in the Finnish study involving 10, 000 men and women []. Flavonoid intake in general was associated with a lower risk of asthma, and the association was attributed mainly to quercetin, hesperitin, and naringenin. Other fruits and vegetables, such as onions, grapefruit, white cabbage, and juices, were not associated with a decreased risk in asthma.

In a study of over 13,000 adults in the Netherlands, it was found that apples might beneficially affect lung function []. Apple and pear intake was positively associated with pulmonary function and negatively associated with chronic obstructive pulmonary disease. Catechin intake was also associated with pulmonary function and negatively associated with chronic obstructive pulmonary disease, but there was no association between tea, the main source of catechins, and chronic obstructive pulmonary disease []. A study of approximately 2500 middle aged (45–59 yrs) Welsh men also demonstrated a beneficial effect of apple consumption on lung function []. Lung function was measured as forced expiratory volume (FEV) in one second, and was positively correlated with citrus fruit, fruit juice/squash, and apple consumption. However, the association with citrus fruit and fruit juice/squash lost significance after adjustment for smoking. Apple consumption remained positively correlated with lung function after taking into account possible confounders such as smoking, body mass index, social class, and exercise. Participants who consumed five or more apples per week had a significantly greater FEV of 138 mL when compared to those who did not consume apples [].

Diabetes and weight loss

Not only may apples help decrease the risk of heart disease, cancer, and asthma, but apple consumption may also be associated with a lower risk for diabetes. In the previously discussed Finnish study of 10,000 people, a reduced risk of Type II diabetes was associated with apple consumption []. Higher quercetin intake, a major component of apple peels, was also associated with a decreased risk in type II diabetes. Myrectin and berry intake were also associated with a decreased risk in type II diabetes, but onion, orange, grapefruit and white cabbage intake were not associated with a lowered risk.

Apple and pear intake has also been associated with weight loss in middle aged overweight women in Brazil []. Approximately 400 hypercholestemic, but nonsmoking, women were randomized to one of three supplement groups: oat cookies, apples or pears, and each subject consumed one of each supplement three times per day for twelve weeks. The participants who consumed either of the fruits had a significant weight loss after 12 weeks of 1.21 kg, whereas those consuming the oat cookies did not have a significant weight loss. Those consuming fruit also had a significantly lower blood glucose level when compared to those consuming the oat cookies [].

Summary

Based on these epidemiological studies, it appears that apples may play a large role in reducing the risk of a wide variety of chronic disease and maintaining a healthy lifestyle in general. Of the papers reviewed, apples were most consistently associated with reduced risk of cancer, heart disease, asthma, and type II diabetes when compared to other fruits and vegetables and other sources of flavonoids. Apple consumption was also positively associated with increased lung function and increased weight loss. Partially because of such strong epidemiological evidence supporting the health benefits in apples, there is increasing research using animal and in vitro models that attempts to more clearly explain these health benefits.

Health benefits and apples: animal and in vitro studies

Antioxidant activity

Apples, and especially apple peels, have been found to have a potent antioxidant activity and can greatly inhibit the growth of liver cancer and colon cancer cells [,]. The total antioxidant activity of apples with the peel was approximately 83 μmol vitamin C equivalents, which means that the antioxidant activity of 100 g apples (about one serving of apple) is equivalent to about 1500 mg of vitamin C. However, the amount of vitamin C in 100 g of apples is only about 5.7 mg []. Vitamin C is a powerful antioxidant, but this research shows that nearly all of the antioxidant activity from apples comes from a variety of other compounds. Vitamin C in apples contributed less than 0.4% of total antioxidant activity.

Antiproliferative activity

Apples have been shown to have potent antiproliferative activity in several studies. When Caco-2 colon cancer cells were treated with apple extracts, cell proliferation was inhibited in a dose-dependent manner reaching a maximum inhibition of 43% at a dose of 50 mg/mL. The same trend was seen in Hep G2 liver cancer cells with maximal inhibition reaching 57% at a dose of 50 mg/mL []. Eberhardt et al. [] proposed that it is the unique combination of phytochemicals in the apples that are responsible for inhibiting the growth of tumor cells. Apples had the third highest antiproliferative activity when compared to eleven other commonly consumed fruits [].

Different varieties of apples had different effects on liver cancer cell proliferation []. At a dose of 50 mg/mL, Fuji apple extracts inhibited Hep G2 cell proliferation by 39% and Red Delicious extracts inhibited cell proliferation by 57%. Northern Spy apples had no effect on cell proliferation []. Apples without peels were significantly less effective in inhibiting Hep G2 cell proliferation when compared to apples with the peel, suggesting that apple peels possess significant antiproliferative activity. Wolfe et al. [] demonstrated that apple peels alone inhibited Hep G2 cell proliferation significantly more than whole apples. For example, apple peels from Idared apples had an EC50 of 13.6 mg/mL whereas the whole apple had an EC50 of 125.1 mg/mL. The EC50 refers to the dose of the apple that is required to inhibit cell proliferation by 50%.

There has been some concern that apple antioxidants do not directly inhibit tumor cell proliferation, but instead they indirectly inhibit cell proliferation by generating H2Oin reaction with the cell culture media []. However, more recently it has been reported that apple extracts did not generate H2Oformation in WME, DMEM, or DMEM/Ham F12 media, and H2O2addition to culture medium did not inhibit Hep G2 cell proliferation or Caco-2 colon cancer cell proliferation []. Additionally, the addition of catalase did not block the antiproliferative activity of apple extracts.

Inhibition of lipid oxidation

Addition of apple phenolics to human serum decreased diphenylhexatriene-labeled phosphatidylcholine (DPHPC) oxidation in a dose dependent manner []. DPHPC is incorporated into low-density lipoprotein (LDL), high-density lipoprotein and very low-density lipoprotein (VLDL) fractions and is an indicator of oxidation. Apple ingestion led to a decrease in DPHPC oxidation, reflecting the apples antioxidant activity in vivo []. The protective effects of apples on LDL oxidation reached its peak at three hours following apple consumption and returned to baseline levels by 24 hours []. Diphenylhexatriene labeled propionic acid (DPHPA) binds to serum albumin and is a good measure of oxidation within the aqueous phase of human serum. Mayer et al. (2001) also found that consumption of apples also led to a decrease in albumin DPHPA oxidation, reaching peak activity at 3 hours.

Although apple juice typically contains less phenolics than whole apples, it is still a widely consumed source of dietary antioxidants. Pearson et al [] examined the effects of six commercial apple juices and Red Delicious apples (whole apples, peels alone, and flesh alone) on human LDL oxidation in vitro. LDL oxidation was measured using headspace analysis of hexanal produced from copper-induced lipid oxidation in vitro. The dose of the apple juices and whole apple, apple peel and apple flesh, were standardized for gallic acid equivalents, and each LDL solution was treated with 5 μM gallic acid equivalents for each apple sample. LDL oxidation inhibition varied greatly between brands of fruit juice, ranging from 9 to 34% inhibition and whole apples inhibited LDL oxidation by 34%. Apple peels inhibited LDL oxidation by 34%, while the flesh alone showed significantly less inhibition (21%) [].

Rats fed apple juice also had a decreased level of malondialdehyde (MDA), a marker of lipid peroxidation []. Quercetin, a major flavonoid in apples, had no effect on lipid oxidation when ingested by rats, suggesting that quercetin alone is not responsible for the apple’s ability to inhibit lipid oxidation []. Other antioxidants and the interaction between the different apple antioxidants, including quercetin, may contribute to the antioxidant activity of apples. The effect of apple juice on lipid oxidation has also been examined in vivo in human subjects. In a study involving four women and one man, ingestion of high levels of a 1:1 mixture of apple juice and black currant juice increased the antioxidant status of the blood and decreased lipid oxidation []. Glutathione peroxidase also increased in humans consuming apple juice. Plasma MDA decreased over the seven-day intervention period when the subjects ingested the highest dose of the apple juice and black currant mixture (1500 mL). Despite the antioxidant effect on lipoproteins, apple juice intake had a pro-oxidant effect on plasma proteins in both humans and rats [,].

Cholesterol-lowering effects

Some of the apple’s protective effect against cardiovascular disease may come from its potential cholesterol-lowering ability. Aprikian et al. (2001) found that when cholesterol fed rats were supplemented with lyophilized apples, there was a significant drop in plasma cholesterol and liver cholesterols and an increase in high-density lipoproteins (HDL). Furthermore, they found that cholesterol excretion increased in the feces of rats fed apples, suggesting reduced cholesterol absorption []. In a second study, a similar cholesterol lowering effect was seen in cholesterol fed rats when rats were fed apples, pears, and peaches. Apples had a greater cholesterol lowering affect than the other two fruits []. The three fruits also increased the plasma antioxidant potential, with apple having the greatest effect []. Apples, pears, and peaches all had similar fiber content, but apples contained more phenolic compounds suggesting that perhaps the phenolics in apples contribute to this effect [].

In obese Zucker rats, apple consumption lowered cholesterol and low-density lipoproteins (LDL), however in lean rats, apple consumption did not change cholesterol levels []. In rats supplemented with cholesterol, apple pomace fiber and sugar beet fiber, the plasma lipids were significantly lower than in rats without the dietary fiber []. Rats fed sugar beet pulp fiber and apple pomace fiber, but not fed cholesterol, had no change in lipids, suggesting that these sources of dietary fiber have hypolipidemic effects only in rats fed cholesterol []. The sugar beet pulp fiber and the apple pomace fiber did not have an effect of lipid peroxides.

Aprikian et al. [] in more recent studies, found that combined apple pectin and apple phenolic fractions lowered plasma and liver cholesterol, triglycerides, and apparent cholesterol absorption to a much greater extent than either apple pectin alone or apple phenolics alone []. This work suggests that there is a beneficial interaction between fruit fiber and polyphenolic components and also supports the benefits of eating whole fruits as opposed to dietary supplements.

Other health effects

Aside from chronic disease, apples may be used to help combat other prevalent disease in the world. Recently it has been found that crude extracts from immature apples actually inhibited enzymatic activities of cholera toxin in a dose dependent manner []. Additionally, apple extract reduced cholera toxin induced fluid accumulation in a dose dependent manner []. The apple extracts were fractionated and each fraction was tested for inhibitory action on enzymatic activities of cholera toxin. The two apple extract fractions that contained highly polymerized catechins inhibited cholera toxin catalyzed ADP-ribosylation by 95% and 98%. The fraction containing non-catechin polyphenols caused only 3.5% inhibition and the fraction containing monomeric, dimeric, and trimeric catechins caused 39% inhibition [].

Summary

Overall, the animal studies and in vitro work begin to define mechanisms by which apples may help prevent chronic disease. First, the strong antioxidant activity of apples may help prevent lipid and DNA oxidation. Cancer cell culture work has demonstrated that apples inhibit cell proliferation in vitro, which may contribute to the association of apple intake with decreased cancer risk. Apples significantly lowered lipid oxidation both in humans and rats and lowered cholesterol in humans. These effects, which may be attributed to both the phenolics and the dietary fiber found in apples, may partially explain the inverse association of apple intake and risk of cardiovascular disease.

Apple phytochemicals

Apples contain a large concentration of flavonoids, as well as a variety of other phytochemicals, and the concentration of these phytochemicals may depend on many factors, such as cultivar of the apple, harvest and storage of the apples, and processing of the apples. The concentration of phytochemicals also varies greatly between the apple peels and the apple flesh.

Some of the most well studied antioxidant compounds in apples include quercetin-3-galactoside, quercetin-3-glucoside, quercetin-3-rhamnoside, catechin, epicatechin, procyanidin, cyanidin-3-galactoside, coumaric acid, chlorogenic acid, gallic acid, and phloridzin (Figure  (Figure2).2). Recently researchers have examined the average concentrations of the major phenolic compounds in six cultivars of apples. They found that the average phenolic concentrations among the six cultivars were: quercetin glycosides, 13.2 mg/100 g fruit; vitamin C, 12.8 mg/100 g fruit; procyanidin B, 9.35 mg/100 g fruit; chlorogenic acid, 9.02 mg/100 g fruit; epicatechin, 8.65 mg/100 g fruit; and phloretin glycosides, 5.59 mg/100 g fruit [].

Figure 2

Structures of selected apple antioxidants.

The compounds most commonly found in apple peels consist of the procyanidins, catechin, epicatechin, chlorogenic acid, phloridzin, and the quercetin conjugates. In the apple flesh, there is some catechin, procyanidin, epicatechin, and phloridzin, but these compounds are found in much lower concentrations than in the peels. Quercetin conjugates are found exclusively in the peel of the apples. Chlorogenic acid tends to be higher in the flesh than in the peel [].

Because the apple peels contain more antioxidant compounds, especially quercetin, apple peels may have higher antioxidant activity and higher bioactivity than the apple flesh. Research showed that apples without the peels had less antioxidant activity than apples with the peels. Apples with the peels were also better able to inhibit cancer cell proliferation when compared to apples without the peels []. More recent work has shown that apple peels contain anywhere from two to six times (depending on the variety) more phenolic compounds than in the flesh, and two to three times more flavonoids in the peels when compared to the flesh. The antioxidant activity of these peels was also much greater, ranging from two to six times greater in the peels when compared to the flesh, depending on the variety of the apple []. This work is supported by Leontowicz et al [] who found that rats consuming apple peels showed greater inhibition of lipid peroxidation and greater plasma antioxidant capacity when compared to rats fed apple flesh.

Many of these phytochemicals from apples have been widely studied, and many potential health benefits have been attributed to these specific phytochemicals. The procyanidins, epicatechin and catechin, have strong antioxidant activity and have been found to inhibit low density lipoprotein (LDL) oxidation in vitro []. In mice, catechin inhibits intestinal tumor formation and delays tumors onset [,]. Sawa et al. (1999) found that chlorogenic acid has very high alkyl peroxyl radical (ROO•) scavenging activity. Compared to about 18 other antioxidant compounds (including quercetin, gallic acid, α-tocopherol), chlorogenic was second only to rutin []. Since ROO• may enhance tumor promotion and carcinogenesis, chlorogenic acid may add to the protective effect of apples against cancer. Chlorogenic acid has been found to inhibit 8-dehydroxy-deoxyguanosine formation in cellular DNA in a rat model following treatment with 4-nitroquinoline-1-oxide [].

Quercetin is also a strong antioxidant, and is thought to have potential protective effects against both cancer and heart disease. Briefly, quercetin has been found to down regulate expression of mutant p53 in breast cancer cells, arrest human leukemic T-cells in G1, inhibit tyrosine kinase, and inhibit heat shock proteins []. Quercetin has protected Caco-2 cells from lipid peroxidation induced by hydrogen peroxide and Fe2+ []. In mice liver treated with ethanol, quercetin decreased lipid oxidation and increased glutathione, protecting the liver from oxidative damage []. Recently, it has been found that high doses of quercetin inhibit cell proliferation in colon carcinoma cell lines and in mammary adenocarcinoma cell lines, but at low doses quercetin increased cell proliferation (20% in colon cancer cells and 100% in breast cancer cells) []. However, low doses of quercetin (10 uM) inhibited cell proliferation in Mol-4 Human Leukemia cells and also induced apoptosis []. Quercetin inhibited intestinal tumor growth in mice, but not in rats. Low levels of quercetin inhibited platelet aggregation, calcium mobilization, and tyrosine protein phosphorylation in platelets []. Modulation of platelet activity may help prevent cardiovascular disease.

Both animal and cell culture studies show that there is an association between the polyphenolic compounds found within apples and a wide variety of effects that may help prevent chronic disease. This supports the hypothesis that it is the phytochemicals found in fruits, especially apples, that impart healthy benefits. More research is still needed to clarify the effects of these compounds in vivo. In order to examine the effects of these compounds in vivo, it is necessary to understand the bioavailability of the specific compounds, and the bioavailability of these compounds within the fruit matrix.

Bioavailability of phytochemicals

As the link between diet and chronic disease grows stronger, many are working to understand how phytochemicals may provide health benefits. An important question to be asked is: Are these phytochemicals bioavailable? Concentrations and bioavailability of phytochemicals are important issues to evaluate when characterizing the effects of dietary phytochemicals on human health. To this date, little literature exists that addresses the bioavailability of phytochemicals from whole foods, including the apple. One of the few studies addressing bioavailability from apples or apple products looks at the bioavailability of polyphenolic compounds from alcoholic apple cider in humans []. After drinking 1.1 liters of apple cider, no quercetin was found in the volunteers’ plasma. Instead, low levels of 3′-methyl quercetin and 4′-methyl quercetin were seen within 60 minutes following consumption of the cider. Caffeic acid was rapidly absorbed, but within 90 minutes the caffeic levels in the plasma were undetectable. Catechin, epicatechin, and phlorizin were not seen in the plasma, possibly because the concentration in the cider was too low. Hippuric acid and phloretin were both increased in the subjects’ urine following the consumption of the cider, but there was no evidence of quercetin, catechin, or epicatechin in the urine [].

In another study involving human subjects, quercetin bioavailability from apples was only 30% of the bioavailability of quercetin from onions []. In this study, quercetin levels reached a peak after 2.5 hours in the plasma, however the compounds were hydrolyzed prior to analysis, so the extent of quercetin conjugation in the plasma is unknown. The bioavailability differences between apples and onions most likely are from the differences in quercetin conjugates in the different foods. Onions contain more quercetin aglycone and more quercetin glucosides, whereas apples tend to contain more quercetin monoglycosides and quercetin rutinoside, which may be less bioavailable. Our lab has examined the bioavailability of both quercetin and quercetin-3-glucoside from apple peel extracts and onion extracts in Caco-2 cells. Apple peel extracts contained no free quercetin, and no quercetin accumulation was seen in the Caco-2 cells following incubation with apple peel extract. Low amounts of quercetin-3-glucoside were absorbed by the cells (4%). However, onions contain some free quercetin and greater amounts of quercetin glucosides, and the absorption of quercetin into the Caco-2 cells from onion extracts was much greater than from apple extracts.

The above results can be explained by recent research examining quercetin and quercetin glycoside bioavailability. In a study by Walle et al. [], it was found that, in the ileostomy fluid, quercetin primarily existed as the aglycone form. The group hypothesized that β-glucosidases hydrolyzed quercetin glucosides to quercetin, which could be then passively transported []. In support of this theory, Day et al. [] determined that quercetin glycosides were mainly deglycosylated by lactase phlorizin hydrolase before the aglycone then passed into the cell. Some intact glycoside transport by SGLT1 occurred and the glucosides were deglycosylated within the cell by cytosolic β-glucosidase. Quercetin-3-glucoside appeared to utilize only the lactase phlorizin hydrolase pathway, not the SLGT1 transporter, but quercetin-4-glucoside used both pathways []. Apples contain some quercetin-3-glucoside that, following hydrolysis by LPH, would be available for uptake by intestinal cells. However, apples also contain other conjugates such as quercetin rhamnosides, quercetin xylosides, and quercetin galactosides that are not easily hydrolyzed by lactase phlorizin hydrolase, and most likely are not readily absorbed by small intestinal cells. In comparison, the quercetin in onions is almost all in the form of quercetin glucosides and free quercetin, making it more bioavailable to small intestinal cells.

Some bacterial degradation of quercetin conjugates most likely occurs in the human intestinal tract. Enterococcus casseliflavis and Eubacterium ramulus, microorganisms isolated from human feces, were both found to degrade quercetin-3-glucoside as a carbon and energy source []. Enterococcus casseliflavis utilized only the sugar moiety of the glucoside, whereas Eubacterium ramulus was also capable of degrading the aromatic ring system with phloroglucinol produced as an intermediate [].

Phloridzin, the glucoside conjugate of phloretin, is the major dihydrochalcone found in apples. Similarly to quercetin glucosides, phloridzin is thought to be hydrolyzed by lactase phloridzin hydrolase, and phloretin aglycone is taken up by the intestinal cells. When rats were fed phloridzin and phloretin, their plasma contained glucuronidated and sulfated phloretin but no phloridzin []. This supports the theory that phloridzin is hydrolyzed prior to uptake and further glucuronidation by intestinal epithelial cells. Phloridzin is known to be a potent SGLT1 inhibitor, but recently it has been discovered that phloridzin is also transported by SGLT1 []. However, phloridzin, as well as other flavonoid glucosides such as quercetin glucoside, is also effluxed by the multi-drug resistance protein (MRP1) [].

In human ileostomy subjects, chlorogenic acid absorption was approximately 33%, and only traces of chlorogenic acid was found in the urine []. The majority of chlorogenic acid will reach the large intestine and may be metabolized by the gut microflora. Gonthier et al (2003) found that rats fed chlorogenic acid excrete very little chlorogenic acid in their urine, but instead they excrete mainly microbial produced metabolites of chlorogenic acid, such as hippuric acid and m-coumaric acid []. A more recent study by Olthof et al (2003) involving human subjects showed that half of the ingested chlorogenic acid was converted to hippuric acid in the colon, most likely by microbial metabolism [].

Catechin and epicatechin are both absorbed by small intestinal epithelial cells []. In contrast to quercetin, epicatechin was not glucuronidated by human liver microsomes, nor was it glucuronidated by human small intestinal or large intestinal tissue []. Both liver and intestinal tissues contain UDP-glucuronosyltransferases (UGT) that are involved in the glucuronidation of various other flavonoids. Epicatechin was found to be sulfated by the human liver and intestinal cytosols, indicating that sulfation is the major metabolic pathway for epicatechin metabolism [].

The mechanisms concerning the bioavailability of specific apple phytochemicals are becoming clearer as bioavailability research increases. In general, many flavonoid aglycones tend to pass through the intestinal epithelial cells where they are further conjugated. The flavonoid glycosides may be absorbed in small amounts, but most absorption seems to occur following hydrolysis by intestinal hydrolases such as lactase phloridzin hydrolase. Upon absorption these compounds are also conjugated. More research is still needed to understand the bioavailability of compounds from whole foods. The effects of the food matrix, interactions between compounds, digestion and processing on bioavailability of apple phytochemicals are still unknown.

Effects of variety and ripening on apple phytochemicals

Varietal differences

Researchers in our lab have found distinct differences in total phenolic and total flavonoid content between different apple varieties. Of four common varieties used for applesauce (Rome Beauty, Idared, Cortland, and Golden Delicious), Rome Beauty had the highest phenolic content while Cortland apples had the lowest []. Rome Beauty apples also had the highest flavonoid content while Cortland apples had the lowest. However, Idared contained much higher anthocyanins than any of the other varieties []. Anthocyanins are the antioxidant compounds in the fruits that may give fruit a red or blue color. Out of 10 varieties commonly consumed in the US, Fuji apples had the highest total phenolic and total flavonoid compounds (Figures  (Figures33 and  and4).4). Red Delicious apples were also quite high, and the apples containing the lowest amounts of phenolics and flavonoids were the Empire apples and the NY647 apple. Antioxidant activity of apples also differs between different varieties, and was positively associated with the level of total phenolic content. The apple varieties with the higher phenolics tended to have higher antioxidant activity.

Figure 3

Total phenolic content of apple varieties (mean ± SD, n = 3).

Figure 4

Total flavonoid content of apple varieties (mean ± SD, n = 3).

Researchers have found similar variations in phytochemical content between different cultivars of apples. Van der Sluis et al (2001) found that Jonagold apples contained the highest concentration of quercetin glycosides, catechins, and chlorogenic acid when compared to Golden Delicious, Cox’s Orange, and Elstar apples. Golden Delicious had the second highest concentration, while Cox’s Orange and Elstar had the lowest concentrations []. Escarpa and Gonzalez (1998) found that Golden Delicious had the lowest concentration of flavonoids when compared to Reinata, Red Delicious, and Granny Smith apples. Reinata had the highest level of flavonoids, followed by Granny Smith and Red Delicious varieties. Another group looked solely at procyanidin content of four varieties of apples and found that Granny Smith and Red Delicious had the highest procyanidins while McIntosh and Golden Delicious had the lowest [].

Growth conditions

Besides variety of apple, factors such as development and ripening of the fruits may impact phytochemical profiles in apples. Quercetin glycosides, phloridzin, catechins, and chlorogenic acid concentrations in Jonagold and Elstar apples were highest early in the season, and decreased to a steady level during maturation and ripening []. Anthocyanins in Elstar and Jonagold apples started high and decreased in mid-season, but rose rapidly just prior to maturation. Interestingly, this increase in anthocyanin content occurred only in fruits grown in the outer part of the canopy, and not in those grown in the inner part of the canopy. The amounts of quercetin glycosides in both Jonagold and Elstar were also greater in fruit grown in the outer canopy []. Awad (2000) also found that sun exposed fruits (both Jonagold and Elstar) had greater levels of anthocyanins and quercetin glycosides when compared to the shaded fruits, giving more evidence that exposure to sunlight affects these two compounds production []. In general, it can be concluded that improving light exposure for apples may help increase the production of certain phytochemicals. There was no sunlight effect on phloridzin, catechin, and chlorogenic acid.

Plant nutrition

The effect of different nutrients on flavonoids and chlorogenic acid in apples has also been examined. Awad (2002) found that nitrogen fertilization was associated with decreases in anthocyanins, catechins and total flavonoids, and also with decreased percentage of blush in the fruit peels. In Elstar apples, calcium fertilization was associated with an increase in anthocyanins and total flavonoids []. They also examined the effects of applications of different chemicals that may enhance ripening on the formation of different phytochemicals. Ethephon increased anthocyanin production, but did not increase chlorogenic acid or any of the other phytochemicals studied. Gibberellins and (s)-trans-2-amino-4-(2-aminoethoxy)-3-butenoic acid hydrochloride (ABG-3168) both decreased anthocyanin production, but did not have an effect on other compounds studied. The application of other chemicals, such as alar, cycocel, seniphos, shikimic acid, plantacur-E and galactose did not have an effect on any of the phytochemicals examined [,].

Effects of storage and processing on apple phytochemicals storage

Apple phytochemical content is not greatly affected by storage. Quercetin glycosides, phloridzin, and anthocyanin content of Jonagold, Golden Delicious, Red Delicious, Elstar, and Cox’s Orange apples were not affected by 52 weeks of storage in controlled atmospheric conditions. Chlorogenic acid and total catechins decreased slightly in Jonagold apples. Total catechin concentration decreased slightly in Golden Delicious, but chlorogenic acid concentrations remained stable []. After 25 weeks of cold storage, there was no decrease in chlorogenic acid in any variety of apple, but catechin content decreased slightly in Golden Delicious, Elstar, and Cox’s Orange apples. Both types of storage had no effect on antioxidant activity in any variety of apple examined. Another group looked specifically at the effects of storage on apple peel phenolics and found that storage at 0°C for 9 months had little effect on phenolic content []. Lattanzio et al. (2001) found that after 60 days of cold storage the concentration of total phenolics in the skin of Golden Delicious apples increased. After 100 days, the total phenolics in the skin began to decrease, but even after 200 days in storage, the total phenolics were similar to those at the time of harvest [].

Processing

Processing of apples has been found to affect phytochemical content. Apple juice obtained from Jonagold apples by pulping and straight pressing had 10% of the antioxidant activity of fresh apples, while juice obtained after pulp enzyming had only 3% of antioxidant activity. After pulp enzyming, the juice contained 31% less phloridzin, 44% less chlorogenic acid, and 58% less catechin. Most of the compounds remained in the apple pomace []. Similarly, Guyot et al. (2003) found that 42% of total phenolics were extracted in the juice, leaving over half the total phenolics in the apple pomace. They found that hydroxycinnamic acids and dihydrochalcones showed the greatest extraction yields in the juice, 65% and 80 % respectively. Procyanidins had the lowest yield in the juice (32%) []. Apple phenolics, especially procyanidins, have been found to bind with cell wall material, which could lead to the decreased levels of polyphenols found in apple juices [].

Apple pomace is a major waste product accumulated mainly during apple juice processing. Phloridzin, chlorogenic acid, epicatechin, and quercetin glucosides have all been isolated from apple pomace []. These phenolics isolated from apple pomace have been found to have high antioxidant activity suggesting that apple pomace may have dietary health benefits and commercial use []. Millions of pounds of waste apple peels are generated in the production of applesauce and canned apples in New York State each year. Since apple peels contain a majority of the antioxidants when compared to the flesh [], apple peels have the potential to be a value-added ingredient in food products. Apple peels were blanched and then dried under a variety of conditions (oven dried at a range of temperatures between 40° and 80°, air dried, or freeze dried). The freeze-dried samples had the greatest total phenolic and flavonoid content, and the total phenolic and flavonoid was actually greater than in the fresh peels. The apple peel powder had strong antioxidant activity and also greatly inhibited cancer cell proliferation [].

Conclusion

In numerous epidemiological studies, apples have been associated with a decreased risk of chronic diseases such as cardiovascular disease, cancer, and asthma. In vitro and animal studies have demonstrated that apples have high antioxidant activity, can inhibit cancer cell proliferation, decrease lipid oxidation, and lower cholesterol, potentially explaining their role in reducing risk of chronic disease. Apples contain a wide variety of phytochemicals, many of which have been found to have strong antioxidant activity and anticancer activity. The interaction of the many apple phytochemicals warrants more study as researchers attempt to further explain the mechanism behind the apple’s ability to reduce risk of chronic disease. Recent research has shown that apples do contain bioavailable phytochemicals, although more work is needed to better understand the bioavailability of phytochemicals within the apple matrix as opposed to pure phytochemicals.

Many factors affect the phytochemical profile of apples, and are important to consider as one attempts to understand and maximize the health benefits of apples. Phytochemical concentrations vary greatly between different cultivars. The level of some phytochemicals varies during maturation of the fruits in response to available light, stage of fruit development and to some types of fertilization. In general, storage of apples does not seem to greatly affect apple phytochemicals, but the processing of apples for juice results in a very significant decrease in phenolics. Processed apple peels retain their phenolic and flavonoid compounds activity and therefore may be used as a value-added ingredient with potent antioxidant activity.

The potential health benefits of apples are numerous. Regular consumption of fruits and vegetables, including apples, as part of a healthy diet may aid in the prevention of chronic disease and maintenance of good health.

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  • Schneider H, Schwiertz A, Collins M, Blaut M. Anaerobic transformation of quercetin-3-glucoside by bacteria from the human intestinal tract. Arch Microbiol. 1999;171:81–91. doi: 10.1007/s002030050682. [PubMed] [Cross Ref]
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  • Walle T, Walle K. The beta-D-glucoside and sodium-dependent glucose transporter 1 (SGLT1)-inhibitor phloridzin is transported by both SGLT1 and multidrug resistance-associated proteins 1/2. Drug Metab and Dispos. 2003;31:1288–1291. doi: 10.1124/dmd.31.11.1288. [PubMed] [Cross Ref]
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  • Awad M, Wagenmakers P, de Jager A. Effects of light on flavonoid and chlorogenic acid levels in the skin of Jonagold apples. Scientia Hort. 2001;88:289–298. doi: 10.1016/S0304-4238(00)00215-6. [Cross Ref]
  • Awad M, de Jager A, Westing L. Flavonoid and chlorogenic acid levels in apple fruit: characterisation of variation. Scientia Hort. 2000;83:249–263. doi: 10.1016/S0304-4238(99)00124-7. [Cross Ref]
  • Awad M, de Jager A. Relationships between fruit nutrients and concentrations of flavonoids and chlorogenic acid in Elstar apple skin. Scientia Hort. 2002;92:265–276. doi: 10.1016/S0304-4238(01)00290-4. [Cross Ref]
  • Awad M, de Jager A. Formation of flavonoids, especially anthocyanin and chlorogenic acid in Jonagold apple skin: influences of growth regulators and fruit maturity. Scientia Hort. 2002;93:257–266. doi: 10.1016/S0304-4238(01)00333-8. [Cross Ref]
  • Goulding J, McGlasson B, Wyllie S, Leach D. Fate of apple phenolics during cold storage. J Agri Food Chem. 2001;49:2283–2289. doi: 10.1021/jf0015266. [PubMed] [Cross Ref]
  • Lattanzio V, Di Vinere D, Linsalata V, Bertolini P, Ippolito A, Salerno M. Low temperature metabolism of apple phenolics and quiescence of Phlyctaena vagabundaJ Agric Food Chem. 2001;49:5817–5821. doi: 10.1021/jf010255b. [PubMed] [Cross Ref]
  • van der Sluis A, Dekker M, Skrede G, Jongen W. Activity and concentration of polyphenolic antioxidants in apple juice. 1. effect of existing production methods. J Agric Food Chem. 2002;50:7211–7219. doi: 10.1021/jf020115h. [PubMed] [Cross Ref]
  • Guyot S, Marnet N, Sanoner P, Drilleau J. Variability of the polyphenolic composition of cider apple (Malus domestica) fruits and juices. J Agric Food Chem. 2003;51:6240–6247. doi: 10.1021/jf0301798. [PubMed] [Cross Ref]
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Articles from Nutrition Journal are provided here courtesy of BioMed Central

How to Store Your Apples

FRUIT AND VEGETABLES: HARVESTING, HANDLING AND STORAGEA. K. Thompson, Pages: 373–443, 2007

Published Online : 30 NOV 2007, DOI: 10.1002/9780470751060.refs

Gut bacteria and mind control: to fix your brain, fix your gut!

Brain-friendly gut bacteria grow well when you eat essential foods.



Gut Bacteria Are Important for your Health

I’m going to try and inform you a little bit about what goes on in your gut. In particular, all the microbes that live in your gut. I will tell you why microbes are so important for your health. Under some conditions, microbes can actually cause quite a severe disease.
 
So there’s been a significant shift in our understanding of what causes disease.
We’ve always thought of disease has to do with who we are, our genes, and then the things we do as we go through life. Now we know that lifestyle keeps us healthy or causes disease. Lifestyle is what we eat and what we get exposed to in the environment.
But what’s apparent now is that in the middle of this and that may be involved in interpreting a lot of these things that we do and eat, is that our gut microbes have a direct link to our genetic material and they can in turn influence how we react and respond to things in the environment and how
1:11
they can keep us healthy or or not and
1:14
really the understanding of gut microbes
1:17
has really taken a fantastic leap since
1:21
around 2000 this graph here shows the
1:24
number of scientific articles that have
1:26
been published about gut microbes and
1:28
you see they really started to take off
1:31
here around 2002 and that’s because of
1:35
Technology so before 2002 the only way
1:38
we could really identify and
1:41
characterize I’ve got microbes was by
1:43
what we could culture on a petri dish
1:45
and since we now know that about 80
1:48
percent of our gut microbes can’t be
1:50
cultured that really isn’t a good
1:51
representation of what’s in our gut but
1:54
then with the advent of gene sequencing
1:56
technology we can now identify microbes
2:00
according to their genetic blueprint and
2:02
what’s apparent is that different types
2:04
of bacteria have a unique genetic
2:06
fingerprint so if we can identify the
2:08
fingerprint we can say whether or not
2:10
they’re present or absent and this as I
2:13
said has led to this huge explosion in
2:14
this area of research we can now
2:16
identify microbes we can
2:18
culture and so this has led to massive
2:21
interest in gut microbes and some of
2:24
these are very recent so the Daily Mail
2:28
thinks that healthy gut bacteria might
2:31
be linked to anxiety and then we’ve got
2:33
others that linking gut brain connection
2:35
autism probiotics as a means of treating
2:38
diseases and then a couple of books this
2:41
one has just come out and those of you
2:43
in the Institute will notice the
2:44
significance of broccoli on the front as
2:46
the Institute is responsible for
2:49
generating strains of broccoli that have
2:52
lots of nutrients good beneficial
2:54
nutrients in them but really the message
2:57
here is that what we eat influences our
3:00
microbes which in turn can influence our
3:02
brain function and keeping it normal but
3:05
as always we have to be aware of the
3:09
hype okay so whenever we read these
3:13
articles we need to have a couple of
3:15
things in mind that allow us to
3:17
determine whether or not you know
3:18
there’s some factual basis to it or
3:20
whether it’s hype and these are some of
3:23
the questions that I would say you need
3:25
to ask so the obvious one is well so
3:27
what do these differences they’re
3:31
detected do they really matter are the
3:34
changes a cause or a consequence of the
3:37
disease and of course we want to know
3:39
how it works what’s the mechanism so is
3:41
there anything in this article that
3:43
allows us to understand how it actually
3:45
works and then a lot of experiments are
3:47
carried out on animals because we can’t
3:49
do many interventions in humans for
3:51
ethical reasons
3:52
so another aeneas question is well is a
3:55
mouse a small human no it isn’t so we’ve
3:58
got to bear that in mind and then
3:59
obviously we’ve got to think all is
4:01
there something else they haven’t looked
4:02
at which could explain what they’re
4:04
describing so behavior in lifestyle
4:07
are two important things so I’m going to
4:09
try and sort of touch on some of these
4:11
things in the rest of my talk so this is
4:14
what I’m going to cover I think I need
4:16
to introduce the gut to you I’ll talk a
4:19
little bit about microbes some
4:20
interesting facts a little bit of trivia
4:22
and then how gut microbes may play a
4:26
role in determining what we eat and what
4:28
the consequences of what we are for our
4:30
health
4:31
well being and then how we actually
4:33
might manipulate they’ve got microbes to
4:35
improve or restore our health so that’s
4:38
what I call lawn care right start with
4:41
so did the guts mouth to the anus it’s a
4:45
long tube here’s a picture taken with an
4:49
endoscope and you can see it’s not as
4:51
smooth tube it’s got these ridges to it
4:54
the muscles this is what allows food to
4:56
be propelled through the guts but it’s
4:59
not a smooth chew it has lots of finger
5:02
like projections that we call villi that
5:04
stick into the lumen to capture
5:07
nutrients and absorb them so the tube is
5:11
quite long it’s like nine meters from
5:13
mouth to anus and somebody has taken the
5:18
trouble trying to calculate what the
5:19
surface area of all these villi are and
5:22
the outcome of that is it’s probably
5:24
about the size of a badminton court so
5:27
it’s an incredibly large area and it has
5:30
to be large in order to take up the
5:31
nutrients that are in your diet to keep
5:33
you healthy and then we also consider
5:37
the process of digestion and the gut is
5:39
in fact a massive bioreactor so we take
5:43
in foods plant material for examples and
5:46
they’ve broken down first of all in the
5:48
small intestine here where the small
5:51
simple sugars are absorbed and then the
5:54
larger more complex plant material that
5:57
we eat in our diet passes through into
6:01
the large bowel or the colon where it’s
6:03
fermented and it’s fermented by the
6:06
bacteria that live in the colon and the
6:09
end product of all of this is something
6:11
called short chain fatty acids which are
6:14
very important because they can provide
6:16
about 5 to 15 percent of our daily
6:19
energy requirements in some animals it’s
6:22
up to 30% so this has to be a very
6:25
efficient process to keep us alive
6:27
basically and the enzymes that are
6:30
responsible the proteins that digest
6:32
these food material and the
6:36
polysaccharides now we only have about
6:39
20 genes in our whole genome that will
6:43
allow that encode proteins
6:44
we’ll break down these carbohydrates but
6:46
one bacterial species this one in
6:49
particular Bacteroides has 260 and you
6:53
think there are thousand species so
6:55
that’s a vast number of proteins that
6:58
can digest the digest our food so the
7:01
bacteria that live in our colon are
7:02
ideally suited for processing our food
7:05
and extracting the maximum level of
7:08
nutrients from them so it’s a bioreactor
7:11
a little bit about the microbes so the
7:15
gut is packed full of microbes there is
7:17
no space that endoscope image I showed
7:20
you they’ve displaced and rinsed out all
7:23
the bacteria normally that will be
7:24
jam-packed with bacteria most of them
7:27
are floating free in lumen but a large
7:31
number of them actually make physical
7:33
contact with the cells that line our gut
7:37
so there’s actually some intimate
7:38
Association of these microbes with our
7:41
gut and there are two terms that we you
7:44
may come across we use to describe these
7:46
microbes the microbiota which is to
7:49
describe all the microorganisms that
7:51
live in the gut and there’s the
7:53
microbiome and that’s all the microbes
7:55
plus all their genes combined so
7:58
microbiota microbiome – as you may have
8:01
come across in a lot of these articles
8:04
but individually bacteria incredibly
8:06
small so this is a head of a pen under
8:08
an electron microscope and each of these
8:11
orange dots represents one bacterial
8:14
cell so you can see that you can get
8:17
lots of bacteria on the top on the tip
8:19
of a pin they’re incredibly small but
8:21
well though they’re small they make up
8:24
for that in their vast numbers so we
8:28
have about 10 trillion cells in our body
8:30
but we actually have ten times that
8:32
number of bacteria in our body and so on
8:36
this scale here we have enough cells it
8:37
would fill half of one of our legs all
8:40
the rest of the body will be filled up
8:41
with microbes bacteria and then if we
8:44
think about all the DNA that we have oh
8:47
this is an interesting quote sorry I
8:49
forgot about this this ninja just give
8:51
you an idea of the scope and scale of
8:52
the numbers here of bugs a bacteria in
8:55
our colon so just one linear centimetre
8:58
contains more bacteria than all the
9:00
humans that have ever been born it’s a
9:02
vast number of microbes and then the DNA
9:05
elements this is the big toe okay and
9:09
that represents the DNA in our body that
9:11
is actually ours okay so everything else
9:15
more than 99% of the DNA is bacterial
9:20
DNA so you know just think about that
9:24
that’s actually quite amazing really so
9:26
we are carrying around a lot of DNA but
9:29
very little of it is our own okay now
9:33
this is the audience participation bit
9:35
some trivia how much do you think all
9:39
the microbes in our body way don’t be
9:46
shy PhD students at the back come on how
9:51
much what
9:56
that’s not conferring su nope
10:04
anybody else kilogram closer to
10:10
kilograms two to three kilograms a lot
10:15
right a couple of bags sugar and if you
10:18
put it in a volume size about one and a
10:20
half liters and there’s about a thousand
10:25
different species thousand different
10:27
types packed in there and this is what
10:30
they need to keep them healthy about 50
10:33
to 65 grams of these things which are
10:36
sugars to keep them healthy so that
10:39
amount is needed every day just to keep
10:42
your microbes healthy and then you’ve
10:43
got all the other things that you need
10:45
to keep your body healthy and so a
10:48
product of all this metabolism is gas
10:54
so how much do you think we expel every
10:58
day and this is everybody so it’s not
11:00
just old men and teenagers everybody in
11:05
this room expelled gas how much do you
11:08
think we expel every day how many liters
11:16
how many five that’s a bit high anybody
11:20
else
11:24
one two four that’s a lot and of course
11:28
at the end of all this we have waste so
11:32
60% of your stool is made up of bacteria
11:35
live and dead okay so that’s trivia
11:41
interesting thing just before you have
11:43
your meal you can run through some of
11:44
these facts and figures but they are
11:47
very very important and we know they’re
11:49
very important because of animals that
11:52
we can keep germ-free so these are
11:54
animals that have never been exposed to
11:56
any microbes they’re sterile and when we
11:59
examine these animals they’re clearly
12:02
compromised they’re deficient so they
12:04
have nutritional deficiencies they don’t
12:07
grow but interesting they live longer so
12:11
if you want to live longer don’t eat
12:12
that’s the bottom line they have a
12:15
defective gut so their gut is not poor
12:17
properly formed so it’s leaky and their
12:21
immune system is very poorly developed
12:22
so they’re very susceptible to
12:24
infections and in fact if you introduce
12:27
a pathogen to these animals it can kill
12:29
them very quickly because they have no
12:31
protection no immunity and also their
12:34
development is affected as well so
12:37
clearly we’re already starting now to
12:38
move into the gut brain so that there
12:41
are really poor animals very sick so the
12:45
microbiota and the Mike Michaels are
12:47
very important so your microbiota is
12:51
unique to you it’s your identity it’s
12:54
like your fingerprint your microbes are
12:56
unique to you however the microbes you
13:01
have are shared with other family
13:03
members so there’s some commonality
13:05
there and interestingly looking at
13:08
the microbiota of monozygotic and
13:11
dizygotic that side entacle non
13:13
identical twins you know there’s no
13:15
difference so even if you’re an
13:16
identical twin you’ll have similar
13:18
differences in your microbiota to non
13:20
identical twins so what does that mean
13:22
well it means that genes are important
13:24
who you are is important but also the
13:28
nurture the nature the nurturing is also
13:30
important in shaping the microbes but we
13:36
now know that we all have a core
13:39
microbiota so there’s about 57 species
13:42
of bacteria that we all share and there
13:45
are two types that predominate in all of
13:47
us here and not unsurprisingly
13:50
these are concerned because they perform
13:53
important functions such as ones here
13:57
degradation of carbohydrates are
14:00
degrading our plant material we eat they
14:03
also provide these fatty acids that we
14:05
need to keep us alive every day and also
14:08
amino acids and vitamins which we can’t
14:10
produce but our gut bacteria can so it’s
14:13
not surprising there’s a core that all
14:15
of us need to keep us healthy but then
14:17
everything else all the other 800 of
14:21
2,000 species are all unique to us so
14:26
where do they come from well your
14:28
parents in particular your mother so if
14:30
you think you have bad bacteria you can
14:32
blame your parents fully justified okay
14:37
now originally it was thought that we
14:40
were born sterile but that’s changing
14:42
slightly is now evidence that we can in
14:44
fact babies do get exposed in the womb
14:48
to bacteria that the mother has and that
14:50
can be through the placenta and also by
14:53
other routes but by far the biggest
14:55
source or time point at which you get
14:58
exposed to microbes is soon after birth
15:01
because if you believe we are born still
15:04
then the bacteria can colonize very very
15:06
quickly so the first few months after
15:09
birth you’re rapidly being colonized by
15:11
bacteria the types of bacteria depend on
15:14
the delivery so if it’s vaginal delivery
15:17
then most of the microbes that will
15:18
colonize the baby will come from the
15:20
mother
15:21
if it’s a c-section then the bacteria
15:23
actually come from the people in the
15:26
operating theater handling the baby and
15:28
most of those will be skin type bacteria
15:31
and that’s important because there are
15:33
now evidence that links later onset of
15:38
various diseases and disorders back to
15:41
whether or not you are vaginally born or
15:43
from a c-section and the types of
15:45
microbes that initially colonize the
15:46
body other things that will impact on
15:49
the types of microbes that will colonize
15:51
this infant are delivery so it’s a
15:54
normal birth or is it just require
15:57
intensive care the age at birth is also
16:00
important is it a full-term birth or
16:02
preterm birth and hygiene obviously
16:05
where you’re born the home versus the
16:07
hospital at very different population of
16:09
microbes that can colonize the infant
16:11
and then after that things that will
16:15
impact and cause alterations in the
16:17
microbes are antibiotics and again it
16:20
depends on how many what types and for
16:23
how long and also very important is
16:25
nutrition whether or not the infant’s
16:28
breast or bottle fed and again the
16:31
breast milk contains lots of ingredients
16:35
including microbes which can colonize
16:36
that baby and keep them healthy but as
16:41
we go older we get exposed to micro some
16:44
other sources and by different routes so
16:46
via the nose and lungs we breathe
16:48
microbes in the mouth and the gut
16:50
obviously the things we eat and through
16:52
the skin and these are the sources so
16:55
water and the food we eat will contain
16:59
microbes we have pets if we live in a
17:02
farm we’re getting exposed to microbes
17:05
from the animals that we live with where
17:08
we live do we live in the country or do
17:10
we live in the city the population of
17:12
microbes again are very different and
17:15
then the type of accommodation or the
17:17
dwelling that you live in you know is it
17:19
single dwelling is it multi-dwelling all
17:21
these people are contributing microbes
17:23
that will you’ll be exposed to and then
17:28
are you indoors or outdoors are you
17:31
active are you inactive are you an Xbox
17:34
fan
17:34
or are you out playing football these
17:36
things will all expose different types
17:40
of microbes all of these are important
17:42
because beyond three years of age your
17:44
microbiota is pretty much set for life
17:47
so the early years of life are critical
17:50
for the development of a healthy
17:51
microbiota however there are cultural
17:55
things and social things that will also
17:57
impact on the types of microbes that
18:00
that populate us now here’s a fact most
18:04
you probably didn’t know okay
18:09
interesting one to experiment on
18:14
so intimacy and you know it’s across the
18:19
animal kingdom different types of
18:20
interests me transfer of microbes
18:24
grooming it’s another one nurturing food
18:33
sharing right we often sit down at the
18:35
table and eat together and we can be
18:37
sharing food it’s a good way of
18:39
transferring microbes and then there’s
18:42
something that’s slightly less you know
18:45
Pleasant but animals do transfer
18:48
microbes to their offspring via this
18:50
route by regurgitation of food and
18:52
transfer food as well as microbes so the
18:56
message here is if you have some good
18:57
bacteria you need to share it because
19:00
there are some of us poor less fortunate
19:03
people scientists for one right I mean
19:07
my wife is very fond of telling me I
19:09
have very little culture so maybe my
19:11
culture is my bacteria so share your
19:14
good bacteria if you have them right so
19:18
we have our microbiota we’ve been
19:20
exposed we’ve got a stable population
19:22
but it’s not the end of the story they
19:24
do change and here we’ve got a
19:27
representation of aging so here you can
19:30
see these circles the different colors
19:32
represent different types of microbes as
19:33
we age you can see the colours change as
19:36
the populations change and there are
19:39
some differences between formula-fed and
19:41
breastfed babies transition to solid
19:44
food is a big one in terms of shifts in
19:46
microbial populations
19:48
and then you can see as we age there is
19:52
an also shift as well in the population
19:54
ageing has an impact in itself but one
19:58
of the most striking impacts is through
20:00
antibiotic treatment and this slide just
20:04
illustrates the impact of antibiotic to
20:07
antibiotics to treat Clostridium
20:09
difficile which is a severe infection
20:11
that is often acquired in hospital so as
20:15
a result of the outgrowth of this
20:17
bacteria we get sick
20:19
so we administered vancomycin or
20:21
metronidazole and what you can see is
20:24
the diversity the number of bacteria we
20:27
have in our gut is drastically reduced
20:28
because the antibiotics have killed them
20:30
all but it’s also killed off Clostridium
20:33
difficile which is a good thing but you
20:35
know there’s a consequence of this in
20:36
that we’ve wiped out a lot of our good
20:38
bacteria so too many antibiotics for too
20:42
long have a very profound and can be a
20:45
long-lived effect on our microbiota so
20:49
antibiotics could be described as a
20:51
man-made catastrophe however most of the
20:54
antibiotics that are used are used in
20:57
agriculture and in farm animals in
21:00
particular to check infection and solar
21:02
8 growth about 19,000 tons of
21:05
antibiotics are used in agriculture
21:07
every year and of course Antipodes get
21:10
excreted by animals and humans as well
21:12
so they can contaminate streams and
21:15
rivers and then get back into the food
21:16
chain and also giving antibiotics or
21:20
children has its consequences as well so
21:24
in the u.s. by 2 years of age most
21:27
children had at least three courses of
21:29
antibiotics I mean a phenomenal number
21:32
of doses of antibiotics given out in the
21:33
US and what this does is it drives
21:36
bacteria to become resistant and this is
21:39
serious okay so this particular organism
21:43
here mmrsa
21:45
now is resistant to most the antibiotics
21:48
that we have in the pharmacy and more
21:51
than 19,000 people here in the US are
21:54
killed which is much higher than number
21:55
of people dying from AIDS I don’t know
21:57
if you just seen on the news today but
21:59
there’s a UK government
22:01
review group is recommended the
22:03
pharmaceutical and it’s invest two
22:04
billion dollars in developing new
22:06
antibiotics there’s a real need for this
22:09
but one of the causes that we administer
22:11
too many antibiotics we take too many
22:13
antibiotics it leads to resistance
22:17
cautionary tale the other side of the
22:19
story is that gut microbes can actually
22:21
work on drugs rather than been affected
22:23
by drugs they can also work on drugs the
22:26
thing to bear in mind is that the vast
22:28
majority of drugs we take are given
22:29
orally and so the microbes in the gut
22:32
can actually alter the drugs they can
22:36
alter their structure they can produce
22:38
factors that interfere with the drugs
22:40
and they can alter how the body reacts
22:43
to the drugs and here are some examples
22:46
so the bad ones are these drugs here
22:49
which are painkillers anti-cancer drugs
22:52
drugs used to control high blood
22:54
pressure in certain individuals that
22:57
have certain populations of microbes
22:59
administering of these drugs will lead
23:01
to increased toxicity and we some
23:04
antibiotic as well as a similar story
23:06
well there’s a good side to this as well
23:08
in that got microbes can process drugs
23:11
to make them more active more
23:12
efficacious such as this antibiotic here
23:16
and this anti-inflammatory drug so what
23:19
this means is that how you react to a
23:21
drug can depend on the type of microbes
23:24
you have in your gut and one of the
23:26
things that medicine is heading towards
23:27
perhaps is being able to administer or
23:30
prescribe you a drug based on the
23:32
population of microbes in your gut
23:33
because there’s no point in giving you a
23:35
drug that your microbes will make toxic
23:38
you want microbes to actually help the
23:41
drugs become better for you more
23:43
efficacious so this is what’s been
23:46
called personalized medicine the drugs
23:48
will be given to you because you have
23:50
been determined to respond best to those
23:53
drugs so then that brings me to really
23:57
the the meat of my talk here in a way
23:59
and this is what I’m going to try and
24:02
persuade you of that your gut microbes
24:05
can now influence what you eat when you
24:07
eat and what happens when you do eat and
24:09
so I formulated this hypothesis
24:14
that gut microbes influence their hosts
24:17
food choices and I sort of put up three
24:19
predictions in order to prove the
24:22
hypothesis could be correct the first
24:24
one is that the microbes you have in
24:26
your gut is a consequence of the food
24:30
that you eat and how you behave in the
24:32
environment so this interesting so it’s
24:36
not a map of the galaxies it’s actually
24:39
the results of screening them the micro
24:42
biomes in a lots of different animals
24:43
and this is sort of a zoo collection
24:45
each dot represents similar microbiota
24:50
in populations of animals and the lines
24:53
of separation here indicate how similar
24:55
or related they are to other micro
24:59
biomes and other animals so we’ve got
25:01
these sequences we know all the microbes
25:04
and this is how they all cluster so you
25:06
can see different clusters so horses and
25:10
rhinos are up here in their own little
25:12
cluster ruminants such as sheep and cows
25:20
make their own cluster elephants are
25:25
their own little grouping up here and
25:29
then we have the carnivores for the
25:31
lions and bears again they’re a
25:32
different cluster in red and then we
25:35
have leaf eating monkey serve vegetarian
25:37
monkeys and pigs and then the other
25:41
primates humans include we’re here so
25:44
we’re separate from the leaf eating
25:46
monkeys so what does this mean well it
25:50
means that who we are and what we eat
25:52
determines heavily influences the
25:56
microbes that populate our gut and
25:57
that’s reinforced by this study in
26:00
looking at the microbes that are present
26:03
in the gut of people that live in
26:06
Burkina Faso in Africa that have a rural
26:09
diet primarily vegetarian based diet and
26:11
Europeans and this is actually Italians
26:13
have a Western diet you can see just
26:15
looking at the colours they’re very
26:17
different ok and what’s interesting is
26:21
if that people in Africa migrated to
26:24
Europe to Italy and then adopt the
26:27
Western
26:28
they lose this and become this
26:32
distribution of microbes so they haven’t
26:35
changed terms their genes or anything
26:36
all they’ve done is that diets changed
26:38
and it’s causes profound shift in the
26:41
microbes so the diet really is a driving
26:44
force in making up the microbes that you
26:47
have in your gut there’s another example
26:49
this is a Burmese python so they go
26:52
through periods of fasting and then
26:53
feasting just looking at three different
26:56
types of bacteria in the fasting state
26:58
you can see very low levels but if
27:01
they’re given a meal you know within
27:03
half an hour you can see these striking
27:05
chips and expansions and increases in
27:10
certain types of bacteria and these will
27:12
eventually stabilize and then hours of
27:14
the animal goes back into a fasting
27:15
state they will decline again so fasting
27:19
reduces the overall diversity and then
27:22
feasting expands the diversity in
27:25
response to diet it’s a quite striking
27:27
so–that’s diet stress is another thing
27:32
we have to cope with in our environment
27:34
and this is some evidence that links
27:37
stress impacting on our gut microbes so
27:42
noradrenaline norepinephrine and effort
27:44
in which all polyp adrenaline are
27:47
produced in response to stress and that
27:49
can have a direct effect on the bacteria
27:52
that live in our gut and it can cause
27:55
the outgrowth the particular types of
27:56
bacteria so here for example ten
27:59
thousandfold increasing growth in
28:01
response to Adrenaline’s produce under
28:03
stress and surgery is a stress and this
28:08
bacteria here rapidly expands following
28:11
surgery and if it’s not contained then
28:14
it can cause sepsis and mice that get
28:18
exposed to a type of stress rapidly
28:20
change their microbial populations and
28:22
that’s just shown here so these are
28:24
normal animals in most the bacteria
28:26
little circular shapes but then under
28:29
food deprivation which is a form of
28:31
stress you know they rapidly changed the
28:33
rod-shaped bacteria and that was
28:35
observed over 40 years ago so we’ve
28:39
known for a while that stress is a major
28:40
factor
28:41
and then what’s interesting is that
28:45
probiotic bacteria that are present in
28:47
some of these health foods is well for
28:52
Morrison’s and this is Actimel they
28:54
contain bacteria that produce a
28:56
neurotransmitter called gaba and gammas
28:59
normally producing the body what it does
29:01
is it dampens down excitable neurons so
29:05
it relaxes you so and this is being used
29:10
by the pharmaceutical industry to
29:12
develop mimics of gamma so they can
29:14
overstimulate these receptors to make
29:16
you even more relaxed and in fact even
29:19
knock you out
29:21
because anesthetics can work by
29:23
mimicking the gaba that is produced by
29:26
these bacteria so benzodiazepines
29:29
alcohol right we all feel nice and
29:31
relaxed after a glass of wine or a
29:34
bottle of beer well you know one of the
29:36
ways that comes out about is that
29:38
they’re stimulating these receptors that
29:41
gut bacteria can do as well so the gut
29:43
bacteria can already you know hopefully
29:46
take us from a stressful state to a
29:49
relaxed straight state and so one of the
29:54
other things i wanted to highlight here
29:55
was this obesity lots of evidence in the
29:58
literature now and in the newspapers
30:00
that changed in our gut microbes to make
30:03
come acres of obese so gut microbes and
30:07
obesity so very this is a very
30:11
interesting experiment probably the best
30:12
experiment that demonstrates how
30:16
microbes can influence whether or not we
30:19
are be so lean so here we have identical
30:22
twins but one of the twins is obese and
30:25
one is lean so we’ve taken the stool
30:28
sample from each of these extracted the
30:30
bacteria what we’ve done is we put them
30:33
into mice the mice are then put on a
30:36
regular diet low-fat high-carbohydrate I
30:41
mean low-fat high-fiber diet the ones
30:44
that got the mic micros and the obese
30:46
twin become obese but the mice that got
30:50
the microbes from the lean twin stay
30:52
lean so that’s a direct call
30:55
all link okay so that’s not really
30:56
height that’s a bit more close to fact
30:59
so of course it’s my slits not humans
31:01
but this is the best evidence we have to
31:03
date that shows the direct causal link
31:05
between our gut microbes influencing
31:08
whether or not we stay lean or whether
31:10
become obese and then this was in the
31:12
Sunday Times this week this was from a
31:16
study carried out by Tim spectra at
31:18
King’s College London and he fed his son
31:21
I don’t know if his son was a willing
31:23
volunteer a high fat diet for 10 days
31:26
Big Macs and lots of coke and then he
31:31
was taking stool samples before an art
31:32
of it the 10-day diet and what happened
31:35
what he showed was that first of all is
31:37
a reduction in nutrients because he’s
31:39
now eating this very processed refined
31:42
foods there was a loss in number he’s
31:45
got microbes but he gained two kilos in
31:48
weight in just 10 days so the
31:51
interpretation of this is that highly
31:53
processed foods present in Big Macs
31:56
containing grease are toxic to certain
31:59
microbes and this leads to a loss of
32:03
diversity we’re losing microbes because
32:06
of this and if you want to know more
32:08
this individual has produced his book I
32:12
had nothing to do with it so I’m not
32:14
doing buy it or anything but if you want
32:16
to know more these books here so loss of
32:19
diversity is a recurring theme and in
32:22
fact I’ve already said in aging we have
32:25
this loss of diversity we lose richness
32:28
we lose microbes the same in obesity and
32:31
it’s the same in other disease in flicks
32:33
inflammatory bowel disease and Crohn’s
32:35
disease so the loss of diversity and
32:38
types of Micra 7 I got is not good it
32:42
can have quite profound health effects
32:44
and so it’s not just got diseases all of
32:48
these diseases shown here are linked by
32:51
a common theme in a change or shift in
32:55
the population of microbes in the gut
32:57
and generally that shift means less
33:00
diversity interestingly quite a few are
33:03
linked with diseases of central nervous
33:06
system nearly
33:07
generative diseases the heart the liver
33:11
fat and rheumatoid arthritis there’s
33:14
lots and this is a lot of complete list
33:16
by any means so obviously well is there
33:19
one microbe or one population of
33:21
microbes that can cause these diseases
33:23
so it’s like looking for Waldo found him
33:30
yeah there is the only problem is there
33:38
are lots of Waldo’s and so it’s probably
33:40
not one microbe it’s the combination of
33:43
microbes that when they get together you
33:45
know it’s a bit like a gang of teenagers
33:47
you know they could be rowdy or it can
33:48
be miserable and anti-social so it’s the
33:53
population when they come together that
33:55
they causes or is probably responsible
33:58
for the effects on our health it’s not
34:00
one it’s probably lots okay so moving on
34:04
to the predictions we’re now at the
34:05
second one so gut bacteria can by
34:09
influencing how our body works influence
34:11
our appetite and food preferences so I’m
34:15
sure this is a familiar scenario for
34:17
many of you you know our mind says no
34:19
take the healthy option but there’s
34:21
something inside of us and I really like
34:23
that piece of cake okay and it may be
34:25
that gut feeling you know I really am
34:28
hungry for a piece of pie rather than an
34:31
apple so what is the evidence that
34:35
normal gut microbes can influence brain
34:37
development and behaviors that’s what
34:39
we’re talking about brain development
34:40
behavior so this is next this is a
34:42
summary of an experiment carried out a
34:44
few years ago looking at our germ-free
34:46
mice again these are sterile Mice and
34:48
mice that have populations got microbes
34:51
this here shows the expression of an
34:54
anxiety related gene so the yellow
34:57
identifies high levels in the brains of
35:01
these mice that have got microbes but
35:04
very little expression in germ-free mice
35:06
and this maze here is a measurement of
35:09
how curious adventurous mice are so if
35:13
they’re cautious timid they’ll spend
35:16
most of their time in the enclosed
35:18
section away from the light but if
35:20
they’re adventurous like
35:21
this one you know they’ll be on the open
35:23
arms so what this study showed was that
35:26
gut microbes can affect normal brain
35:29
development and make these mice more
35:33
curious I’m sorry wrong way and perhaps
35:41
more creative and trying to escape
35:44
so it’s this fear extinction you have
35:48
got microbes you become a little bit
35:49
more cautious reticent a little bit more
35:52
anxious if you don’t have got microbes
35:54
you know it’s the Great Escape you’re
35:56
looking for ways out more striking
36:00
experiments this one shown here so we’ve
36:02
got two strains of mice what we’ll call
36:04
timid and adventurous so they’ve got
36:08
microbes of anything to do with why
36:09
these animals are timid or adventurous
36:11
and what we did so not well we did this
36:13
group in Canada did was they took the
36:15
stool from the timid Mouse isolated the
36:18
microbes and put it into an adventurous
36:21
Mouse and that Mouse became timid the
36:25
other way around they took the microbes
36:27
from an adventurous Mouse put it into a
36:31
timid Mouse and these are germ-free mice
36:34
so they’re they’re an empty vessel that
36:35
you can put the microbes into and they
36:37
became now adventurous so this is a
36:40
direct causal link again showing the gut
36:43
microbes can influence the behavior of
36:46
mice at least now is this translatable
36:50
to humans I can see probably some people
36:52
in you always thinking maybe I could
36:54
give this to my husband yeah would he
36:55
still be a grumpy old man if I gave him
36:58
some microbes and would you know if my
37:00
teenage boy had some microbes form you
37:03
know somebody maybe they become bit more
37:05
outgoing bit more social maybe no maybe
37:08
a few years from now maybe I’ll have
37:10
that but not just yet but I mean we
37:14
really shouldn’t be too surprised by
37:15
this because we now know that the gut
37:18
actually contains an awful lot of the
37:20
neurons neural circuitry that’s present
37:22
in the brain and it’s often thought to
37:24
be the second brain I mean it has a very
37:27
large number of neurons 500 million and
37:30
it produces lots of neurotransmitters
37:32
and you know there’s some
37:35
some evidence that sort of links that
37:37
got to the brain so brain-dead people
37:42
their stomach functions normally for
37:43
quite a while it’s almost an inherent
37:45
activity anybody that’s taken paint
37:48
major pain-killing drugs like morphine
37:50
for example you know the risk of
37:52
constipation it shuts down motility in
37:55
your gut and emotions and feeling are
37:58
intimately associate with bowel function
38:00
right we’ve all had their butterflies in
38:02
the stomach that nervous got action well
38:05
that’s all those neurons in your gut
38:07
that are firing away and when you look
38:09
at the structure of the nerves in the
38:11
gut that make up the enteric nervous
38:13
system you know these are the neurons or
38:18
the dendrites here in silver the white
38:20
color this is our gut tissue and you can
38:23
see that when we superimpose these two
38:25
the nerve fibers actually penetrate and
38:28
intermix between all our gut tissue and
38:30
they actually look like they’re actually
38:33
protruding into the lumen to be able to
38:35
sense perhaps the presence of factors
38:38
that they can respond to that are in the
38:40
gut looming that could be made by gut
38:42
microbes and the vagus nerve is
38:46
ultimately this the route by which all
38:49
this signaling in the gut leads into the
38:51
brain so all these signals here that the
38:54
enteric nervous system responds to are
38:57
fed into the brain via the vagus nerve
38:59
and so we know that if the vagus nerve
39:06
is blocked or damaged through injury
39:08
profound effects on appetite and eating
39:12
in fact it causes drastic weight loss so
39:15
it’s clearly a regulator of body weight
39:17
and vagus nerve stimulation by hormones
39:22
and neurotransmitters in the gut could
39:25
drive excessive eating behavior so over
39:27
stimulation is not necessarily good
39:29
thing and not surprisingly gut microbes
39:32
can actually regulate how much of these
39:34
neurotransmitters and hormones are
39:36
produced in the gut and they can
39:38
manipulate this to their own advantage
39:41
by producing things that can block or
39:43
stimulate the
39:45
consistent in the gut so microbes
39:47
control eating behavior by influence
39:49
signals that are delivered to the brain
39:51
and by the vagus nerve and two of the
39:54
most importance of dopamine and
39:56
serotonin so dopamine
39:58
associated rewards pleasure compulsions
40:02
serotonin regulates our mood our memory
40:05
sleep cognition dopamine about half of
40:10
the amount of dopamine producing the
40:11
body is produced in the gut and some gut
40:14
microbes can produce vast amounts of
40:17
dopamine and so you may know that L
40:21
dopamine is used to treat Parkinson’s
40:23
disease serotonin is even more striking
40:26
but virtually all the serotonin the body
40:28
is made in the gut and gut microbes
40:31
produce factors that can mimic or block
40:34
serotonin action in the gut and
40:37
deficiency of serotonin is linked to
40:39
depression so I hope you can see that
40:42
microbes by manipulating just these two
40:45
neurotransmitters can profoundly
40:47
influence our mood behavior whether
40:50
we’re anxious whether relaxed how much
40:52
we sleep how much we eat and so linking
40:58
this to a disease interest this is more
41:00
recent study now linking gut microbes to
41:02
a disease that’s called autism spectrum
41:06
disorder so autism so we know from
41:10
looking at patient’s microbiota is that
41:12
they they have they’re disturbed they
41:15
have alterations the makeup of microbes
41:17
and also there are altered levels of
41:20
what the microbes produce and there’s a
41:23
mouse here that can be can develop
41:26
autism like Syndrome particular
41:28
excessive grooming and vocalization is
41:32
affected as the art as it is in autistic
41:34
children and what this group that works
41:37
with this mouse showed that they could
41:39
restore or treat this mouse by using ant
41:42
probiotics so live bacteria and so the
41:47
live bacteria altered the gut
41:49
composition of the microbes and it
41:50
looked now more like normal animals and
41:53
this was linked to resealing of the gut
41:56
so these animals are leaking
41:58
and it was the leakiness allowing but
42:00
these microbe derived byproducts to get
42:03
into the bloodstream and into the brain
42:04
but as soon as the barrier was improved
42:07
the leakage stopped and it restored the
42:12
normal levels that you would find in
42:13
serum and it stopped or halted some of
42:17
the features of autism so this is animal
42:20
experimentation but it clearly shows
42:22
that it could be a role for alterations
42:25
in gut microbes that are linked to
42:26
neurodegenerative diseases and autism in
42:29
particular so neurotransmitters well
42:33
there are also hormones producing the
42:35
gut which regulate appetite and here
42:38
they said there are appetites that are
42:40
produced to say stop eating you’ve eaten
42:43
too much now we have all we need
42:45
no more tweet and then there are
42:47
hormones it’s signals to the brain state
42:49
we’re hungry you need to eat and it’s
42:52
the balance of these two that determine
42:55
our appetite regulates how much we eat
42:58
when we eat not surprisingly now perhaps
43:01
you think what gut bacteria can alter
43:04
the balance of these hormones and these
43:08
hormones are mainly produced in the gut
43:10
so we know that probiotic bacteria can
43:13
raise the level of this amino acid
43:16
tryptophan and tryptophan is an
43:18
important because it’s involved in
43:20
generating or producing these hormones
43:22
and bacteria that live in the gut can
43:26
produce mimics of some of these hormones
43:30
in for example leptin graylien pyy that
43:35
are influenced your appetite so they can
43:39
influence eating and appetite control
43:41
directly by mimicking the hormones
43:43
normally produced in the gut
43:45
indirectly they can stimulate things
43:47
that will block hormone signaling to
43:50
change your appetite and this is a
43:55
slightly different one this is very
43:57
recent showing how we with this
44:00
information we can actually use it to
44:02
try and redress the balance so here we
44:07
have this chemical here which is
44:09
produced as a result of a break
44:11
digestion of fats is called napes and as
44:15
I said these are naturally producing the
44:16
small bowel as a process of digestion
44:18
lipid digestion obese individuals have
44:22
very low levels compared to normal
44:24
healthy individuals and so what this
44:28
group said well okay what if we engineer
44:30
a bacteria that lives in the gut to
44:31
produce this factor can we then reboot
44:35
increase the levels back to normal and
44:39
so what they show is when they fed these
44:40
bacteria producing this chemical to mice
44:43
you could protect them from becoming
44:45
obese so give them a high fat diet given
44:47
lots of Big Macs
44:48
they stayed lean just by giving bacteria
44:52
that produced this chemical and what’s
44:55
interesting is this persisted for a very
44:58
long time even after the bacteria to
45:00
left the body there was still in effect
45:02
so obviously this could lead to a
45:06
different type of intervention using
45:08
these engineered bacteria as a treatment
45:12
for redressing appetite control and
45:14
maybe even obesity so gut microbes you
45:18
know we can engineer them and we can
45:20
utilize our expertise in work with
45:22
microbes for beneficial effects and you
45:26
know I’ve tried to highlight one or two
45:28
things that microbes produce that
45:29
influence our behavior this is a little
45:31
bit more of a list that shows things
45:33
that impact on our body’s function I’ve
45:36
talked about energy metabolism the
45:38
equity’s factors that help is blood clot
45:40
blood for blood coagulation new
45:43
adjustments I talked about that sleep
45:46
and mood they produce factors that will
45:48
determine how much sleep we take whether
45:50
or not sleeps beneficial and it’s just
45:53
they produce factors that cause bad
45:54
breath so a variety of things that
45:56
impact on our health and behavior so I
46:00
come to the third prediction that there
46:04
is a positive selection system positive
46:07
reinforcement if you like in which the
46:10
type of food we eat selects for specific
46:12
microbes which in turn then feedback on
46:15
making us eat more of that and my
46:18
example here is a seaweed diet so a
46:22
stable diet selects a microbial
46:24
specialists the
46:25
lead to us wanting to eat more of these
46:27
things so there’s two types of seaweed
46:29
Dyer this is one but I’m not going to
46:32
talk about that one I’m going to talk
46:36
about this one okay seaweed now Japanese
46:42
in in Japan vast amounts of seaweed are
46:46
consumed every year about more than four
46:48
kilograms per person but they can
46:52
process and eat seaweed because they
46:55
have genes present in their microbes
46:58
that produce the enzymes that allow them
47:00
to break down the seaweed okay the genes
47:04
originated from bacteria that live on
47:06
the seaweed so as they were consuming
47:09
the seaweed some of those microbes
47:12
stayed in the gut long enough to pass on
47:14
these genes to the normal population of
47:17
microbes in the gut so this microbes
47:22
that contaminated seaweed actually
47:24
transferred some of the beneficial
47:26
enzymes and genes they had to the normal
47:29
population migra’s in their gut so this
47:31
is positive reinforcement because
47:33
seaweed has lots of health benefits the
47:36
exacta fication promotes weight loss
47:38
lowers blood cholesterol so the helps
47:41
reasons to eat it and the more you eat
47:43
the more microbes and genes you have you
47:47
acquire enable you to break it down and
47:49
get maximal nutritional benefit so it’s
47:51
is positive reinforcement but you can
47:54
only do that if you have the microbes
47:57
there and the genes present in the first
47:58
place Japanese population do because
48:02
they consume a lot of that so as another
48:05
type of food preference which is food
48:07
avoidance and food allergy okay
48:10
so food allergies have increased
48:12
dramatically in recent times so more
48:16
than 50% since 1997 and they’ve been
48:19
linked to the modern lifestyle so-called
48:22
hygiene hypothesis overuse of
48:24
antibiotics again destroying of the
48:27
microbiota and so we can sort of look at
48:30
this in more detail using again mice and
48:33
so if we destroy the microbiota in mice
48:35
with antibiotics we can actually
48:38
lick give these mice analogy to peanuts
48:41
just as many children have but if we
48:44
reintroduce one type of bacteria into
48:46
the gut we can actually cure them of
48:48
their allergy and that’s this bacteria
48:50
Clostridium so this is direct evidence
48:53
linking gut microbe activity to food
48:56
avoidance okay and food allergies so not
49:01
only are the microbes that will
49:02
encourage us to eat more there are
49:04
microbes in our gut that will stop us
49:06
from eating things which causes harm
49:08
smart bugs
49:10
really and also sweetness and taste
49:13
again if you look at taste receptors
49:16
that are present on the tongue germ-free
49:19
mice have different types of receptors
49:20
compared to mice that have populated the
49:22
microbes so Joffrey mice have a sweet
49:26
tooth they prefer more sweets and have
49:28
lots more sweet receptors on their
49:30
tongues than mice that have populations
49:35
of michaeles in their gut and so near is
49:37
the knowledge on come to in humans is
49:39
patients that undergo gastric bypass
49:41
surgery for obesity their food
49:44
preference is shift enormously in fact
49:47
they develop avoidance strategies to
49:49
stop eating like some dairy products and
49:51
even meat and this is a company by
49:54
striking change than they got microbes
49:56
as a result of the surgery so microbes
50:00
can influence food preferences by
50:02
altering our taste perception of foods
50:05
so all of this together is summarized
50:09
here so what I’m predicting is that food
50:12
cravings are associated with vagal nerve
50:14
stimulation by blocking that we control
50:17
appetite and we can reduce food cravings
50:20
by altering our gut microbes we can cure
50:24
food cravings and we can cure maybe
50:27
allergies and then the diversity of our
50:31
gut microbiota and what they produce
50:33
should affect food choices and satiety
50:36
okay so if we increase the diversity we
50:39
have a better chance of controlling
50:41
appetite and keeping us healthy and not
50:43
from gaining excessive weight so that’s
50:47
great so how do we actually go about
50:50
changing the
50:51
that live in our gut so this is gut
50:54
microbe therapy which I’m leading to
50:55
lawn care so anything or when’s it going
50:57
to talk about lawn care that’s coming
51:00
right so message to fix your brain you
51:04
need to fix your gut and there are
51:07
different strategies we can use there’s
51:09
the expensive one pharmacy prescription
51:12
of drugs sorry getting a bit ahead of
51:15
ourselves here
51:18
antimicrobial therapy so obviously I’ve
51:21
highlighted some of the issues with
51:23
antimicrobial therapy toxicity can cause
51:27
the outgrowth of pathogens like cross
51:29
stream difficile and we develop
51:32
resistance our bugs would develop
51:33
resistance to the antibiotics and
51:35
they’re not cheap vancomycin however has
51:38
been used for diet induced obesity to
51:40
control diet in use to be so it’s not
51:42
all bad news
51:43
but it’s still expensive other
51:45
approaches rely on biotics Pro and
51:48
prebiotics and then I’m going to talk
51:50
about transplants I there we go I will
51:55
do probiotics there we go live
51:58
microorganisms which when administered
52:01
in adequate amounts confer a health
52:02
benefit that is the w-h-o definition of
52:05
a probiotic they are found in a variety
52:08
of foods these will be most familiar to
52:10
you these are generally for anybody then
52:15
we have ones that are designed for
52:16
children and even pets so you can get
52:19
probiotic to your pets evidence that
52:24
they work or may work so there’s
52:26
evidence that they can decrease food
52:28
intake they can reduce fat mass improve
52:31
insulin sensitivity stop us from
52:33
becoming diabetic yogurt is the food
52:37
that’s most associated with reduce
52:38
weight gain if you think of the things
52:40
that we eat to try and reduce our weight
52:42
yogurt is one of the things we generally
52:44
eat and probiotic treatment in pregnancy
52:48
can prevent excessive weight gain in the
52:51
infant after birth so the other approach
52:55
is prebiotics and prebiotics can be
52:57
suited as food to feed your healthy
53:00
microbes
53:01
and if you go remember back to my gut
53:03
trivia slide I said you need to consume
53:05
50 or 60 grams and these things well
53:08
this is what I’m talking about
53:10
these are the types of food that I will
53:13
fuel provide the fuel for your healthy
53:15
bacteria and there can be in lots of
53:18
things from pre-burn even toothpaste
53:20
contain probiotics prebiotics food for
53:24
your gut bacteria so this is what they
53:26
are generally as I said the different
53:28
types of sugars breast milk is a very
53:31
good source of inulin which is a very
53:33
good prebiotic and then these variety of
53:36
foods here
53:38
but five a day this is one of the reason
53:42
why we keep saying five servings of
53:44
fruit and vegetables a day there are
53:46
very good source of prebiotics to keep
53:48
your gut bugs healthy okay so you can
53:52
take probiotics and you can feed your
53:55
healthy bugs by eating these types of
53:57
foods the more radical approach is okay
54:01
that’s not working let’s get rid of
54:03
everything and replace it so fecal
54:07
microbiota transplantation so this is it
54:11
in a snapshot
54:16
and maybe I’ll cure me a my food
54:18
addiction yeah sounds gross
54:21
God how the hell could this work but it
54:23
does work it works incredibly well for
54:27
treating gut infection against C
54:28
difficile to come up again you know it’s
54:31
a 94 percent cure rate which is much
54:33
much higher than all the drugs and
54:34
antibiotics sounds gross but it works so
54:38
the question why does it work and how
54:40
does it work well that’s something the
54:42
Institute we’re very interested in
54:43
knowing so it works but you might think
54:46
well this is something new I’ve only
54:47
been reading in the Daily Mail for the
54:49
last year or so but in fact it goes back
54:52
a long long way the Chinese were way
54:54
ahead of us so two and a half thousand
54:57
years ago they were giving people yellow
54:58
soup to drink to keep them healthy vets
55:01
have been using it for a couple hundred
55:04
years a post called transformation
55:07
transferring stool from one animal to
55:10
another to keep it healthy first really
55:13
use tested in humans in 1958 it was
55:17
given to four patients there were near
55:19
death from a type of colitis it cured
55:22
all four patients and then since the C
55:25
difficile experiment you know we’ve
55:27
treated over 500 patients no side
55:31
effects whatsoever and success rate is
55:34
incredibly high and it’s stable so as
55:37
far as five years out you know these
55:39
people are still free of Clostridium
55:41
difficile infection so it is very good
55:44
so how do we do it there are several
55:47
options okay there’s the craps you’ll
55:53
there’s you know things you can have
55:56
it’s part of your healthy diet for
55:59
there’s the very more unpleasant way a
56:02
tube and if you go on the internet you
56:05
can get do DIY kits that allow you to do
56:07
this at home
56:08
very scary stuff but you know I think
56:11
we’d all prefer the crap show so what
56:14
are we going to use it for so I’ve said
56:16
you know there’s some obvious diseases
56:17
obesity clearly I’ve shown giving you
56:20
some evidence that got microbes cause
56:22
obesity so if we change our gut microbes
56:24
can we stop us from becoming obese or
56:26
even cause weight loss eating disorders
56:29
again
56:30
showed it as a link between our gut
56:32
microbes and what we eat or what we
56:34
can’t eat so again this could be another
56:36
application autoimmune diseases
56:38
inflammatory bowel disease Crohn’s
56:41
disease ulcerative colitis rheumatoid
56:44
arthritis they’re all potential slightly
56:46
more speculative but something we’re
56:48
interested at the Institute in looking
56:49
at can we reverse some of the effects of
56:51
aging ooh not quite sure what that is
56:59
now I don’t want BT burned so yes can we
57:05
reverse the effects of aging so our gut
57:07
microbes change drastically as we age
57:10
and that’s the search of a decline in
57:12
our immune system function we become
57:14
less resistant to infections and we
57:18
mostly some people here probably annual
57:20
flu vaccines right try and boost our
57:22
immunity
57:23
what if we could boost your immunity by
57:25
giving you a crap seal would you rather
57:28
have a needle or a corruption maybe
57:32
maybe we can reverse other signs of
57:34
aging you know maybe ifr we’re rich and
57:37
famous because we’ve got the youth
57:39
capsule yeah Reggie’s taking orders at
57:43
the frontier
57:45
how does it work well this is another
57:48
example of how it works so this is fecal
57:50
microbiota transplant by a nasal gastric
57:52
tube so this is you know the way it’s
57:54
been working so far taking my crinkle
57:57
micros from lean donors given to
57:59
patients with metabolic syndrome these
58:01
are patients at risk of developing
58:02
diabetes six weeks post treatment we can
58:06
clear glucose from the blood and they’re
58:08
now responding to insulin and this is
58:10
associated with a drastic change but
58:13
they got microbes increased diversity
58:16
but with everything that’s always a bunt
58:19
and this is the butt donor selection is
58:22
important this is a very reason a report
58:25
was published 32 year old female with a
58:29
recalcitrant C difficile infection
58:30
remember this is the disease we can cure
58:33
with FM t she decided she wanted to take
58:37
stool cell from her daughter as the
58:40
donor as you probably would a daughter
58:43
was a little overweight
58:44
but she later gained weight and became
58:47
obese the mother 16 months post
58:51
treatment have been given her daughter’s
58:54
microbes got microbes became obese she
59:00
gained excessive weight despite all
59:02
interventions she could not keep the
59:05
weight off and at 36 months she weighed
59:08
80 kilograms a BMI of 34.5 what this led
59:14
in this particular Hospital was a
59:15
complete change in the way donors are
59:17
selected okay so there is the smoking
59:21
gun here obviously the clinicians would
59:23
think well it came from the best patient
59:25
we just transferred the phenotype to the
59:27
mother well maybe but clear there’s a
59:29
link here so what we have to think about
59:31
carefully now is donor selection what is
59:33
the criteria we need to apply to a donor
59:36
in order to be able to use their stool
59:38
sample for a transplant here’s the lawn
59:43
care so if you think about trying to
59:47
keep your gut microbes healthy you know
59:48
here’s our healthy flourishing lon we
59:51
can devastate it with antibiotics you
59:54
know we can just let the weeds grow so
59:56
if we’ve got antibiotics
59:59
you know we might want to give
60:00
prebiotics you know turf food or we
60:04
might want to put new seed down
60:05
probiotics right and then the more
60:08
radical therapy a lawn transplant
60:11
bacterial therapy okay so think of your
60:14
gut
60:15
keeping Elvis lawn care and this is my
60:19
take-home message okay if you have young
60:23
children get them a pet and let them
60:26
roll around in the mud
60:27
let them eat mud you know maximum
60:30
exposure lots of healthy microbes and
60:34
with that I thank you and I’m happy to
60:36
take any questions you might have
60:37
thank you
60:47
you

Mussels Recipe

A simple and quick mussels recipe is a mussel potato-beet salad.

Mussel potato beet salad

Mussels Recipe:

  1. Wash and boil some potatoes and beets.
  2. Remove from pot when tender
  3. Chop up the potatoes and beets on a plate
  4. Lightly salt the potatoes
  5. Open a can of mussels
  6. Drizzle the mussels and oil over the potatoes and beets.
  7. Eat and enjoy!

Mussels are very nutritious and a great source of vitamin B-12!



Mussel Nutritional Facts:  

Mussel is the common name used for members of several families of bivalve molluscs, from saltwater and freshwater habitats. Wikipedia

Amount Per 

Calories 172
% Daily Value*
Total Fat 4.5 g6%
Saturated fat 0.9 g4%
Polyunsaturated fat 1.2 g
Monounsaturated fat 1 g
Cholesterol 56 mg18%
Sodium 369 mg15%
Potassium 268 mg7%
Total Carbohydrate 7 g2%
Dietary fiber 0 g0%
Protein 24 g48%
Vitamin A6%Vitamin C22%
Calcium3%Iron37%
Vitamin B-65%Vitamin B-12400%
Magnesium9%
*Per cent Daily Values are based on a 2,000 calorie diet. Your daily values may be higher or lower depending on your calorie needs.

 

Prostate cancer prevention diet

Prostate cancer prevention

A recent prostate study showed that participants who consumed at least 10 portions of tomatoes weekly showed an 18% reduced risk of developing prostate cancer. The study concluded that a high intake of plant foods and tomato products, in particular, may help protect against prostate cancer.

Foods for prostate cancer prevention on a dinner plate with white fish cherry tomatoes vegetables

Adherence to dietary and lifestyle recommendations and prostate cancer risk in the prostate testing for cancer and treatment (ProtecT) trial.

Er V, Lane JA, Martin RM, Emmett P, Gilbert R, Avery KN, Walsh E, Donovan JL, Neal DE, Hamdy FC, Jeffreys M
Cancer Epidemiol Biomarkers Prev. 2014 Oct; 23(10):2066-77.


Another study concluded that lycopene, green tea and potentially soy-containing products may be preventative.

Foods for prostate cancer prevention on a dinner plate with white fish, cherry tomatoes, and vegetables

A Mediterranean-style diet rich in monounsaturated fatty acids and vegetables and fruits and low in red meats also helps.

And daily sunshine exposure helps to build up vitamin D stores. In the ProtecT study, deficiency in vitamin D (circulating concentration <12 ng/ml) was associated with a greater risk of aggressive prostate cancer (higher grade or stage),

Foods to Avoid with prostate cancer

A recent meta-analysis of dietary factors and supplements and prostate cancer risk has concluded that foods to avoid are red and well-done meats, fat and milk should be limited.

Previously, the EPIC consortium found an increased prostate cancer risk with the highest quartiles of dairy protein, but no association with dietary fat (mostly using FFQs)., Data from the US Health Professionals study based on clinically detected cases found no association between calcium intake and localised prostate cancer (measured with FFQs) but a positive association with advanced disease.Conversely, calcium intake was related to an increased risk of localised disease with screen-detected cases in the US PLCO trial.

The evidence for a link between obesity and fatal prostate cancer is strengthening and energy intake might be on that causal pathway. An association between energy intake and advanced disease was shown in a meta-analysis for studies with disease stage with a combined odds ratio of 1.6 for advanced disease. In this study, there was no overall relationship between energy intake and prostate cancer nor heterogeneity in the risk of disease by stage (P=0.07); the association with advanced disease was positive (23% increase) but did not reach conventional statistical significance (95% CI 1.00–1.51).

The finding of weak evidence of heterogeneity in the association of vitamin D with risk between clinically and screen-detected disease may merit further investigation. The precision of estimates of foods consumed irregularly, such as oily fish, a good source of vitamin D, may be lower in food diaries than in questionnaires. Vitamin D levels are also related to sunlight exposure, making serological assessments more comprehensive. In the ProtecT study, deficiency in vitamin D (circulating concentration <12 ng/ml) was associated with a greater risk of aggressive prostate cancer (higher grade or stage), which would be more prevalent in clinically detected cases, but the recent meta-analysis does not support vitamin D supplementation, except for deficiency.

There was no association of overall diet (assessed using FFQs) and screen-detected prostate cancer in the US PCPT trial nor in the Swedish study., Food diary data from 133 prostate cancer cases also revealed no association with diet and prostate cancer, but a reduction with a Mediterranean-style diet rich in monounsaturated fatty acids and vegetables/fruits and low in red meats. A recent meta-analysis of adherence to a Mediterranean diet and overall cancer risk showed a 4% risk reduction for prostate cancer incidence.

The natural history of prostate cancer remains poorly understood, including the time points when dietary and environmental factors may influence disease development or progression. This study measured dietary intake prior to diagnosis and found no major associations with prostate cancer risk, yet migrant studies and international variation in prostate cancer incidence suggest that dietary or other environmental components contribute to disease risk. More recent evidence highlights a role of dietary factors in disease progression, for example, fat intake may influence prostate cancer mortality. Future studies will need to extend measurement of dietary intake across the life course, consider intermediary influences such as the insulin-like growth factor axis and examine the role of obesity, which increases the risk of aggressive prostate cancer, subsequent disease progression and mortality.

Conclusions

In summary, this large study revealed no strong evidence that prostate cancer risk is associated with dietary intake measured prior to diagnosis in middle-aged and older men.

Acknowledgments

We thank the participants and diary coding staff for their contributions, and Ms Vanessa Er and Dr Kate Northstone for analytical advice. Professor Sheila Rodwell (known professionally as Sheila Bingham) who died in 2009, established the Dietary Cohort Consortium as Director of the MRC Centre for Nutritional Epidemiology and Cancer. The authors’ responsibilities were JAL, SEO and TJK wrote the manuscript; PNA conducted the statistical analysis and all authors contributed to the interpretation of data and review of manuscript, including the final manuscript. None of the authors had a personal or financial conflict of interest. The sponsors had no role in study design, data collection, analysis and interpretation of results or the writing of the manuscript. Supported by the UK Medical Research Council and the Medical Research Council Population Health Sciences Research Network. The cohorts received funding from the British Heart Foundation; Cancer Research UK (grant number C8221/A19170); the Department of Health, UK; the Food Standards Agency, UK; the Medical Research Council, UK; the Stroke Association, UK and the WCRF. The ProtecT trial is funded by the UK National Institute for Health Research Health Technology Assessment Programme (projects 96/20/06 and 96/20/99) and the nested ProMPT study (Prostate Mechanisms of Progression and Treatment), funded by the National Cancer Research Institute (NCRI – formed by Cancer Research UK, the Medical Research Council and the Department of Health). DK is funded by the UK Medical Research Council (MC_UU_12019/1). The funding sources had no role in the study design, conduct, data collection, management, analysis and interpretation or preparation, review or approval of the article.

Footnotes

The authors declare no conflict of interest.

References

  • Ferlay J, Soerjomataram I, Ervik M, Dikshit R, Eser S, Mathers C et al GLOBOCAN 2012 v1.0, Cancer Incidence and Mortality Worldwide: IARC CancerBase No. 11 [Internet]. Lyon, France: International Agency for Research on Cancer; 2013. Available from http://globocan.iarc.fr (accessed 23 July 2015).
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  • Hjelmborg JB, Scheike T, Holst K, Skytthe A, Penney K, Graff RE et al. The heritability of prostate cancer in the Nordic Twin Study of Cancer. Cancer Epidemiol Biomarkers Prev 2014; 23: 2303–2310. [PMC free article] [PubMed]
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  • Allen NE, Key TJ, Appleby PN, Travis RC, Roddam AW, Tjonneland A et al. Animal foods, protein, calcium and prostate cancer risk: the European Prospective Investigation into Cancer and Nutrition. Br J Cancer 2008; 98: 1574–1581. [PMC free article] [PubMed]
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3 harmful foods to avoid

3 harmful foods to avoid are:

  1. flavored yogurt containing high-fructose corn syrup, modified corn starch, or added sugar,
  2. cereals, and
  3. bread and cakes


Yogurts to Avoid

The ingredients label on a blueberry Danone Activia yogurt, for example, lists ingredients comprising:

Skim milk, sugar (11 g), cream, water, blueberries, modified corn starch, skim milk powder, milk and whey protein concentrate, gelatin, natural flavour, natural colour, active probiotic culture, etc.

Danone Activia yogurt nutrition label with ingredients list: foods to avoid
Danone Activia yogurt nutrition label with ingredients list contains sugar and modified corn starch: foods to avoid

Danone Activia yogurt

Danone Activia yogurt blueberry ingredients

Chocolate to Avoid

Most milk chocolate has a great deal of sugar. Stick with dark chocolate that is at least 70% cocoa.

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Cereals to Avoid

Most cereals contain large amounts of sugar and other types of useless carbohydrates.

breakfast cereals are processed foods to avoid

Cakes to Avoid

Cakes made with sugar are common and they are definitely not good for a daily diet. Some kids eat chocolate cake for breakfast. It is a harmful food choice.

Bread to Avoid

Some bread types are less harmful than others. You want to maximize protein to carbohydrate ratios in bread, cereal bars, snack bars, etc.

Pumpernickel bread contains lots of sugar, so it is a food to avoid. Eating pumpernickel bread and flavored yogurt for breakfast every day will turn most women into fat cows. Pumpernickel bread ingredients comprise:

  • Bread flour,
  • rye flour,
  • cornmeal,
  • salt,
  • yeast,
  • cocoa,
  • brown sugar,
  • milk,
  • oil,
  • and molasses.

Snacks to Avoid

Olean chips, Lays chips, and flavored tortilla chips like Doritos are really bad for you.

Low protein cereal bars, such as Nutri-Grain bars are not meant to be a daily meal replacement. A 37 g bar contains 130 Calories but only 2 g of protein. Most of the calories come from the 25 g of various types of carbohydrates in the bar.

Kelloggs Nutri Grain bars raspberry flavor: foods to avoid

Anything labeled “Low-Fat,” processed food, and anything containing high-fructose corn syrup.

High-fructose corn syrup is 20% sweeter than sugar and it interrupts leptin production. Fructose causes lipogenesis. When fructose is consumed, absolute lipogenesis is 2-fold greater than when it is absent (100:0).   Dietary Sugars Stimulate Fatty Acid Synthesis in Adults

Digestion is Important

If the food that you eat does not agree with your digestive system, it may cause acne, bloating, cramps, diarrhea, or gas. If you experience these symptoms, then eliminate the foods causing problems for your digestive system. Many adults can’t digest milk and cheese. If you can’t digest a food, then stop eating it.

Preservatives prevent you from digesting a food as the bacteria in your gut can’t break it down.

Top Foods to Avoid

  • Bratwurst (contains 50 grams of added sugar in the USA and Canada),
  • Hot Dogs
  • Cakes
  • Chips
  • Grains (Even whole grain bread.)
  • Low protein cereal bars
  • Fast foods (they are packed with preservatives.)
  • Red meat
  • Rice: white rice, basmati rice, brown rice (They all contain arsenic)
  • Sugar (Don’t put it in your coffee, tea, or salad)
  • Olestra (also known by its brand name Olean) is a fat substitute that adds no fat, calories, or cholesterol to products. It has been used in the preparation of otherwise high-fat foods such as potato chips, thereby lowering or eliminating their fat content.
  • Processed foods

Avoid Eating Grains

Grains (even whole grains) will spike your blood sugar higher than pure sugar and imbalance your gut bacteria. Grains mess up your immune system and cause cholesterol issues leading to impaired brain function, insulin resistance and ultimately a host of chronic diseases like diabetes, cancer, arthritis and Alzheimer’s. Grains also contain anti-nutrients that prevent your body from being able to absorb certain important nutrients like calcium. Grains damage your body gradually so most people fail to notice the changes until you actually take it out of your diet to see what happens. Read Grain Brain by David Perlmutter, Kristin Loberg

Ketchup flavored Doritos ingredients in Canada:

Selected corn, vegetable oil, seasoning (sugar, corn maltodextrin, salt, monosodium glutamate, sodium acetate, dehydrated tomato, acetic acid, dextrose, citric acid, malic acid, natural flavour, dehydrated onion, colour, dehydrated garlic, disodium inosinate, disodium guanylate, spices), calcium hydroxide.

Every effort is taken to ensure that the ingredients and nutritional information listed on our website is accurate, however, this information may change from time to time.

References:

  1. Katie J. Astell, Michael L. Mathai, Andrew J. McAinch, Christos G. Stathis, Xiao Q. Su. A pilot study investigating the effect of Caralluma fimbriata extract on the risk factors of metabolic syndrome in overweight and obese subjects: a randomised controlled clinical trial. Biomedical and Lifestyle Diseases (BioLED) Unit, College of Health and Biomedicine, Victoria University, Melbourne, Victoria 3021, Australia.
  2. Niedzielin, K., Kordecki, H.,
    http://journals.lww.com/eurojgh/Abstract/2001/10000/A_controlled,_double_blind,_randomized_study_on.4.aspx
  3. Elizabeth J. Parks4,* Lauren E. Skokan5Maureen T. Timlin6, and Carlus S. DingfelderThe Journal of Nutrition, Dietary Sugars Stimulate Fatty Acid Synthesis in Adults, Published 2008
  4. M. Million, et al. Obesity-associated gut microbiota is enriched in Lactobacillus reuteri and depleted in Bifidobacterium animalis and Methanobrevibacter smithii. International Journal of Obesity (2012) 36, 817–825; doi:10.1038/ijo.2011.153; published online 9 August 2011
  5. Rastmanesh R., et al. High polyphenol, low probiotic diet for weight loss because of intestinal microbiota interaction. Chemico-Biological Interactions, Published 15 October 2010.
  6. Thielecke F, et al. Epigallocatechin-3-gallate and postprandial fat oxidation in overweight/obese male volunteers: a pilot study Eur J Clin Nutr. 2010 Jul;64(7):704-13. doi: 10.1038/ejcn.2010.47.
  7. Wang H., Effects of catechin enriched green tea on body composition. Obesity (Silver Spring). 2010 Apr;18(4):773-9. doi: 10.1038/oby.2009.256.
  8. Bitange Nipa Tochi, Zhang Wang, Shi – Ying Xu and Wenbin Zhang, 2008. Therapeutic Application of Pineapple Protease (Bromelain): A Review. Pakistan Journal of Nutrition, 7: 513-520.
  9. Date K, Satoh A, Iida K, Ogawa H. Pancreatic α-Amylase Controls Glucose Assimilation by Duodenal Retrieval through N-Glycan-specific Binding, Endocytosis, and Degradation. J Biol Chem. 2015 May 28. pii: jbc.M114.594937.
  10. Perano SJ,Couper JJ,Horowitz M, Martin AJ, Kritas S, Sullivan T, Rayner CK. Pancreatic enzyme supplementation improves the incretin hormone response and attenuates postprandial glycemia in adolescents with cystic fibrosis: a randomized crossover trial.J Clin Endocrinol Metab. 2014 Jul;99(7):2486-93. doi: 10.1210/jc.2013-4417. Epub 2014 Mar 26.

Processed foods list

Our processed foods list helps you to avoid eating foods that will produce insulin in your body.

Insulin converts 25% of the calories you consume into fat cells in your body. Insulin prevents you from burning all of the calories you consume each day. As a result, you feel hungry and you feel the need to consume more calories, thereby creating a vicious cycle that makes you want to eat more and more each day. And if you cut back on food, you will feel like you lack the energy to exercise.

  • Processed foods produce insulin in the body.
  • Insulin blocks leptin signals in the brain.
  • Lipogenesis is the metabolic formation of fat.
  • Insulin drives weight-gain.
  • Processed foods are the culprit to explain people’s expanding waistlines.


Fruit Flavored Yogurt

Are you still skeptical? Can’t I still eat my fruit flavored yogurt in the morning? Answer: No. Fruit flavored yogurt doesn’t have real fruit in it. It has fructose. Fructose causes lipogenesis. When fructose is consumed, absolute lipogenesis is 2-fold greater than when it is absent (100:0).   Dietary Sugars Stimulate Fatty Acid Synthesis in Adults 1–3

Watch Dr. Robert Lustig‘s video on hunger and hormones to understand the relationship between processed foods and insulin production.

The term processed foods refer to foods that are packaged in boxes, cans or bags. These foods need to be processed extensively to be edible and are not found as is in nature.

Most yogurt sold in stores also contain trans fats. Trans fats raise your bad (LDL) cholesterol levels and lower your good (HDL) cholesterol levels. Eating trans fats increases your risk of developing heart disease and stroke. It’s also associated with a higher risk of developing type 2 diabetes.

Processed foods list 

  • Artificial ingredients, such as synthetic dyes (like FD&C Red No. 40, Tartrazine, or Blue No. 1) and sweeteners
  • Bacon
  • Beef jerky
  • Bread with more than 4 ingredients (other than seeds)
  • Breakfast cereals, such as Cheerios, Special K, Captain Crunch, etc.
  • Cheese
  • Chopped fruit or vegetables in a package are processed foods
  • Cookies
  • Cream cheese
  • Drinks, such as milk, powdered juices, soft drinks
  • Factory farmed meat and seafood
  • Fast Food
  • Flavored yogurt
  • Frozen prepared foods
  • Fructose
  • Ham
  • Imitation crab meat
  • Low-fat products
  • Margarine
  • Meat, if canned or dried
  • Microwave ready meals
  • Pasta
  • Pop tarts
  • Pudding cups
  • Salads at McDonald’s are full of high-fructose corn syrup and thickeners made from corn
  • Sausages, hot dogs, salami
  • Shortening, soybean oil, and even canola oil
  • Snacks, such as crisps
  • Soups:
    • Annie Chun’s soup
  • Stouffers frozen prepared foods
  • Sugar, corn syrup, cane juice, or brown rice syrup
  • Sweeteners (like saccharin, aspartame, or sucralose).
  • Tinned vegetables
  • White rice
Annie Chun's Miso soup packages
Annie Chun’s Miso soup packages are a processed food

References

Too much fructose can damage your liver, just like too much alcohol

Dietary Sugars Stimulate Fatty Acid Synthesis in Adults 1–3, 2008

Insulin and leptin as adiposity signals, 2004

There is now considerable consensus that the adipocyte hormone leptin and the pancreatic hormone insulin are important regulators of food intake and energy balance. Leptin and insulin fulfill many of the requirements to be putative adiposity signals to the brain. Plasma leptin and insulin levels are positively correlated with body weight and with adipose mass in particular. Furthermore, both leptin and insulin enter the brain from the plasma. The brain expresses both insulin and leptin receptors in areas important in the control of food intake and energy balance. Consistent with their roles as adiposity signals, exogenous leptin and insulin both reduce food intake when administered locally into the brain in a number of species under different experimental paradigms. Additionally, central administration of insulin antibodies increases food intake and body weight. Recent studies have demonstrated that both insulin and leptin have additive effects when administered simultaneously. Finally, we recently have demonstrated that leptin and insulin share downstream neuropeptide signaling pathways. Hence, insulin and leptin provide important negative feedback signals to the central nervous system, proportional to peripheral energy stores and coupled with catabolic circuits.

Effects of sugar on the body

The effects of sugar on the body are multi-fold.

What does “Added sugar” mean?

Any sugar added in preparation of foods, either at the table, in the kitchen or in the processing plant. This may include sucrose, high fructose corn syrup and others; these are all processed sugars. http://sugarscience.ucsf.edu/glossary.html#.WP_NFIjyuUl

The problem with processed sugar , regardless of source, is that the processed (white) sugar has been largely stripped of all it’s normally associated vitamins and minerals. The sugars found in fruit have vitamins, minerals, and fiber associated with them which help your body to metabolize them properly.

Sugar is a neurotoxin

In a 2010 study, Scott Kanoski, assistant professor of biological sciences at Perdue University in the US, showed that as little as three days of a diet that is high in saturated fat and sugar was enough to change cognition in rats. The Effects of a High-Energy Diet on Hippocampal Function and Blood-Brain Barrier Integrity in the Rat

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3409296/

https://www.weforum.org/agenda/2017/03/this-is-the-impact-of-sugar-and-fat-on-your-brain

Sugar destroys your liver:

Sugar acts as a chronic, dose-dependent liver toxin (poison) when consumed in excess, according to Dr. Robert Lustig, professor of Pediatric Endocrinology at the University of California, San Francisco (USCF).

 

http://articles.mercola.com/sites/articles/archive/2016/01/13/sugar-destroys-liver-brain.aspx

Too much fructose can damage your liver, just like too much alcohol

There is growing scientific consensus that the effects of sugar, especially fructose, can be toxic to the liver, just like alcohol.1,2

All carbohydrates contain glucose. Some foods, notably fruits, also contain fructose. Fructose is the sugar that makes fruit taste sweet. For most people, there’s nothing wrong with eating fructose in its natural state, in fruit.

Fructose is sweeter than glucose, so it’s most often used as an added sugar in processed foods, whether in the form of high-fructose corn syrup or just plain old sugar. Fructose is one of the most common types of sugar in the US, Canada, and Mexico.

Sucrose is plain old sugar sucrose: it’s a 50-50 mix of fructose and glucose.

You make high-fructose corn syrup by adding enzymes to cornstarch, a glucose, so it turns into fructose. High-fructose corn syrup contains around 55 percent fructose. It’s an effective sweetener. See the FDA’s article: High Fructose Corn Syrup: FDA Questions and Answers

Manufacturers extract and concentrate fructose from corn, beets and sugarcane. They remove the fiber and nutrients in the process. High doses of fructose are in many processed foods. Unfortunately, many kids and adults eat a variety of processed foods throughout the day. Some people will eat a bag of chocolates and candy in an afternoon. Without fiber to slow it down, the fructose is way too much for our bodies to handle.

A new study, drawing on clinical trials, basic science, and animal studies, finds that fructose is more damaging to health than glucose.

Lucan and DiNicolantonio lay out a series of findings that show the digestive tract doesn’t absorb fructose as well as other sugars. More fructose then goes into the liver. Too much fructose in the liver eventually creates a cascade of metabolic problems that includes fatty liver disease, systemic inflammation, type 2 diabetes, and obesity.

sugar

This issue has been hotly debated, since many say that metabolic problems including diabetes, prediabetes, and obesity stem from eating too many calories, period, or too many calories from sugar regardless of the type.

Fred Brouns, Ph.D., a nutrition professor at the Maastricht University in the Netherlands, has published studies on fructose metabolism. He doesn’t think the evidence supports a claim that the fructose found in a typical American diet deserves to be singled out. It’s never eaten in isolation, for starters.

“Fructose can be detrimental, correct, but only in excessive amounts that are not consumed by the majority of the population. It is unrealistic to put the finger to sugars alone and certainly notto fructose in isolation,” he said in an email.

Michael Goran, Ph.D., a professor of preventive medicine and physiology at the University of Southern California, who has also published papers on fructose, also sees fructose as especially harmful.

31% of American adults and 13% of kids suffer from non-alcoholic fatty liver disease (NAFLD).

If you watch pre-1980s TV, you will be shocked to see that almost everyone was much thinner in those days.

Nearly all added sugars contain significant amounts of fructose.3 Typical formulations of high-fructose corn syrup contain upwards of 50% fructose, depending on processing methods. Table sugar and even sweeteners that sound healthy, like organic cane sugar, are 50% fructose.

http://sugarscience.ucsf.edu/the-toxic-truth/#.WP_NjYjyuUl

UCSF Mini Medical School lecture about sugar by doctor Robert Lustig, MD

Pediatric endocrinologist Robert Lustig, MD gave a UCSF Mini Medical School lecture about sugar and obesity in July 2009. Over 7 million people have watched the YouTube watched the 90-minute video as of April 2017.

“I have been very gratified by both the volume of the response, and the quality of response that the video has garnered,” says Lustig, who serves as director of UCSF’s Weight Assessment for Teen and Child Health, or WATCH, Clinic. “I also have been very touched by the personal testimonials of many patients who have written to me about their own travails.”

In the YouTube video, Lustig argues that the current obesity epidemic can be blamed on a marked increase in the consumption of a type of sugar called fructose over the last 30 years. Fructose is a component of the two most popular sugars: sucrose or table sugar, and high-fructose corn syrup, which has become ubiquitous in soft drinks and many processed foods.

Lustig says that fructose is toxic in large quantities because it is metabolized in the liver in the same way as alcohol, which drives fat storage and makes the brain think it is hungry.

“People are searching for answers to this epidemic that make sense,” he says. “The science of fructose metabolism in the liver and fructose action in the brain turn the normal cycle of energy balance into a vicious cycle of consumption and disease.

“What I have proposed is quite controversial; that our food supply has been adulterated right under our very noses, with our tacit complicity. But I think the public gets it, and the tide is turning.”

Read more about the UCSF Lecture on Sugar & Obesity Goes Viral as Experts Confront Health Crisis at http://www.ucsf.edu/news/2010/03/3222/ucsf-lecture-sugar-and-obesity-goes-viral-experts-confront-health-cri