Alcohol – Bad News for Good Bacteria

We’ve looked previously 1 at recent research revealing that any amount of alcohol intake is associated with certain types of cancer. We’ve also looked in some detail at how important bacteria (the microbiota 2 ) in our intestines 3 4 5 6 7 8 , bladder 9  and mouth 10 are for our physical and mental health. But what about the effect of alcohol (beer, wine and spirits) on the health of our microbiota?

You can find any amount of industry-funded research extolling the benefits of having a glass of red wine (that it contains polyphenols like resveratrol 11 , for instance). You will hear ‘conventional wisdom’ that it’s good to have “all things in moderation“.

But the microbes 12 within our bodies don’t listen to such pleasant reassurances.

Increasing amounts of research is providing us with a clearer understanding of how our favourite tipple affects the precious microbiota, which in turn has significant effects on our short- and long-term health.

Let’s get the alcoholics out of the way

However you want to define an alcoholic, it’s not going to be a shock to anyone that their microbiota are going to suffer if they consume vast quantities of alcohol, either on a regular basis of moderate to high intake or in less regular ‘binges‘ of high intake. And this is what’s shown in the following research.

A May 2012 study 13 compared the microbiota composition of groups of a non-alcoholic control group and an alcoholic test group (including individuals with and without alcoholic liver disease).

Study results

Dysbiosis (also called dysbacteriosis) refers to a microbial imbalance or maladaptation. This study found marked differences in the balance of various species/families of microbiota between the healthy control group (HC), those alcoholics without alcoholic liver disease (ALD) and those alcoholics with liver disease (ALD):

In this particular chart, the bacteria family called Bacteroidaceae, generally thought of as being beneficial to health, can be seen as reduced in the ALC and further reduced in the ALD group. There were additional differences found in the ratio of other dysbiotic and nondysbiotic bacterial communities between members of the two alcoholic groups (ALC and ALD) – including decreases in Clostridia and increases in Bacilli and Gammaprotoebacteria in those alcoholics described as having dysbiotic microbiota.

Study conclusion

“…the community composition of the dysbiotic cases is very different from those within the nondysbiotic cases, suggesting an overall disarray of the gut bacterial microbiome in the dysbiotic cases…we show that chronic alcohol consumption is associated with altered dysbiotic microbiota composition in a subset of alcoholics. We report that the alcoholics with dysbiosis had lower median abundances of Bacteroidetes and higher ones of Proteobacteria 14 . When the study subjects are examined according to study group, the alcoholic groups had a reduction in abundance of Bacteroidaceae.

Thus, not all alcoholics studied had such unhealthy microbiota that they could be defined as dysbiotic; however, all alcoholics (ALC and ALD) had less ‘good’ and more ‘bad’ bacteria in their guts than the non-alcoholic control group (HC). The health effects of this type of imbalance have been shown in previous blogs (referenced above) to be linked to a wide range of diseases.

Further research on general alcohol consumption

A 2015 review 15 looked at the effect of alcohol consumption on the microbiota in the gastrointestinal tract (GIT).

 Causes of GIT dysbiosis (chart is from this 2015 study)

The authors considered that alcohol-induced changes in the composition (quantitative and qualitative) and metabolic function of the GIT microbiota are likely contributors to:

  • alcohol-induced oxidative stress
  • intestinal hyperpermeability 16 to luminal bacterial products
  • endotoxemia 17
  • subsequent development of alcoholic liver disease (ALD)
  • other organ pathologies
  • increased GIT inflammation
  • systemic inflammation
  • tissue damage
  • as well as other diseases
               GIT bacterial changes in alcoholics (chart is from this 2015 study)

The reviewers recommend that gut-directed interventions, such as probiotic 18 and synbiotic 19 modulation of the intestinal microbiota, are solutions that should be considered and evaluated for the prevention and treatment of alcohol-associated pathologies.

Study conclusions

The researchers state that: “Chronic alcohol consumption causes intestinal dysbiosis in both rodent models and humans. Dysbiosis in the intestinal microbiota may contribute to the pathogenesis of liver disease…

There’s no precise definition of ‘chronic’ in this study; thus, I’m left uncertain about whether it ranges from those who enjoy a couple of glasses of wine every evening to those who either regularly or occasionally consume vast quantities of alcohol.

Whatever the definition, they conclude that chronic consumption:

  • alters intestinal barrier function, which is shown to lead, for example, to
    • gut leakiness
    • production of proinflammatory & pathogenic microbial products
    • negatively-affected liver metabolic pathways 20

“…Thus, understanding the effect of alcohol on intestinal microbiota composition, may lead to a better understanding of its future functional activity, with the ultimate goal to restore intestinal microbiota homeostasis.

Discussion

How much and how often we need to drink alcohol in order to start causing a leaky gut is something that this study does not specifically cover. Thus, so far, those of us who consider that we are not alcoholics, but simply enjoy a regular or occasional drink, don’t really need to worry about all this stuff. But we still have more research to look at before we can reassure ourselves so easily… After all, the working assumption of WFPB nutrition is that it’s wise to be suspicious of anything that’s not a whole food – and alcoholic drinks are certainly not whole foods.

Since this latter study looked at ways in which probiotics can be manufactured and sold (for profit, of course), it’s worth pointing out that good healthy plant food already contains all the prebiotics and probiotics that most people require. All whole plant food comes with millions of beneficial bacteria which are usually all the probiotics we need; and all unprocessed plants come pre-packed with all the fibre we normally need – and prebiotics are simply types of fibre found only in plant foods, and never in animal foods. Indeed, we saw previously 21 that there are concerns about the safety and efficacy of commercially-prepared probiotics 22 .

Alcohol & Leaky Gut

A 2003 study 23 looked at how alcohol consumption leads to disturbances in the intestinal absorption of nutrients, including several vitamins. The inhibition of the absorption of sodium and water caused by alcohol consumption contributes to the tendency in heavy drinkers to develop diarrhoea.

The study points out that even a single episode of heavy drinking can result in “…duodenal erosions and bleeding and mucosal injury in the upper jejunum [the part of the small intestine between the duodenum and ileum]…The mucosal damage caused by alcohol increases the permeability of the gut to macromolecules. This facilitates the translocation of endotoxin and other bacterial toxins from the gut lumen to the portal blood, thereby increasing the liver’s exposure to these toxins and, consequently, the risk of liver injury.

They conclude that “..recent experimental studies support the assumption that alcohol significantly modulates the mucosal immune system of the gut.

These findings on the effects of single episodes of binge drinking (which is defined as having 4 or more alcoholic drinks within a short period of time) have been supported by additional studies 24 .

Discussion

It’s not just chronic alcoholics who can experience leaky gut; it appears that the weakening of the delicate intestinal membrane, and thus the passage of toxins into the bloodstream, can happen after just one heavy drinking session. There’s no indication in this study about the effects of moderate but regular consumption of alcohol, nor of which type of drink (wine, beers, spirits) have the most damaging effects.

Gut microbiota and leaky gut

It appears that a major part of the reason why alcohol consumption can lead to a leaky gut is because of the alterations alcohol makes to the gut microbiota (or gut flora, as it’s also called). This can lead to ‘bacterial translocation’ 25 which, in turn, can cause inflammatory changes in the liver and elsewhere within the body.

A 2008 study 26 considered the mechanisms involved when alcohol exposure leads to increased intestinal permeability. This is shown in the diagram below:

They point out that alcohol exposure has the ability to promote growth of Gram negative bacteria in the intestine. This is important because it may lead to the accumulation of endotoxins 27 . In addition, alcohol metabolism by Gram negative bacteria and intestinal epithelial cells 28 can result in accumulation of acetaldehyde 29 , which in turn can increase intestinal permeability to endotoxins.

They also point out that alcohol-induced generation of nitric oxide may also contribute to increased permeability to endotoxin. The endotoxin, having permeated the gut membrane, passes to the portal vein which, in turn, carries endotoxin to the liver where it binds to Kupffer cells and initiates a cascade of events leading to teh production of TNF-α (Tumour Necrosis Factor-α is a cell signalling protein (cytokine) involved in systemic inflammation) and subsequent liver injury.

And the damage does not end there. Endotoxin that escapes to the general blood circulation may then induce injury to other organs. For instance, a part of TNF- α produced in the liver may reach to intestine via bile duct or general circulation and further increase intestinal permeability to endotoxin.

Discussion

The health of the liver is closely related to the health of our gut bacteria. The above explains some of the mechanisms involved in liver and other organ damage due to the gut leakage as a result of alcohol consumption. Again, there is no clear definition of the quantity or frequency of alcohol consumption that’s needed in order to trigger these mechanisms.

Location matters

A February 2016 study 30 , discussed in some detail in a Scientific American article 31 adds more information about the process by which alcohol consumption (particularly heavy consumption) negatively affects the microbiome. The study found that: “Disease often depends not on the presence or the total amount of an organism in the gut but rather on location, which in this case is the gut mucosa.

They did experiments on mice and found that if alcohol is given to the mice, some important genes (Reg3b and Reg3g) are downregulated 32 . The result of this is that they then produce significantly less of the antimicrobial molecules that can protect the gut against gram-negative and gram-positive organisms.

The mice given alcohol developed more (bad) bacteria in their guts and more severe liver disease compared with normal wild-type mice whose Reg3b and Reg3g genes had not been affected by alcohol.

Location is important in humans as well as in mice

The researchers also looked at samples of human gut tissue taken during colonoscopies: “Sure enough, heavy drinkers had more bacteria in their mucosa, just as was seen in the mouse model. That suggested the alcohol was suppressing production of the naturally protective peptides.

When bacteria gets into the mucosa, they can then leak through the epithelium wall into the bloodstream (leaky gut): “The balance between microbes and immune defenses was upended and more bacteria were able to migrate through the gut wall into the body, eventually traveling through the bloodstream to the liver. T cells attacked the invaders and the resulting inflammation scarred the liver.” They are going to further investigate which type of microbes are most dangerous if they migrate into the bloodstream; at the moment, this study is basically looking at quantity rather than type of microbes in the mucosa.

Study conclusion

A product delivered to the middle of the gut may have little benefit; it may have to be packaged in a way to hone in on the mucosa. Potential treatments, however, are years if not decades away. Until then the best thing people can do is reduce alcohol consumption to lessen possible damage to the body.

Discussion

The researchers were looking for some genetic or pharmaceutical means of treating genetic/microbial changes caused by heavy alcohol consumption, and their findings suggest that simply using a treatment that flushes the gut, without being targeted into the mucosa, will have little effect. As you can see from their conclusion, they don’t expect any magic pill to be invented before years, possibly decades, have passed. So their suggestion about erring on the side of caution by reducing alcohol consumption seems sensible.

What they don’t look at is whether diet can reverse or in any way affect the situation where a heavy drinker has inadvertently caused a microbial build up in the mucosa within their gut. My suspicion is that the body is capable of repairing itself if it is given the appropriate nutrients (without continuing with the onslaught of the damaging alcohol, of course) over an extended period of time – weeks to months of a non-SOS WFPB diet.

Study shows a few days of alcohol use causes damage

Plenty of studies 33  have looked at long-term alcohol use, whilst a March 2017 study 34 focused on the changes that would happen if mice were given a controlled amount of alcohol for a period of 10 days.

Akkermansia bacteria reduced by alcohol consumption

The number of Akkermansia bacteria were found to be dramatically reduced by alcohol consumption. Other studies 35 corroborate this finding.

So what?

This genus of bacteria in gut barrier maintenance is disrupted by alcohol.

Taxonomic Rank

A parallel decrease in population numbers of Akkermansia has also been found to be decreased in mouse models of obesity and type-2 diabetes, while supplementation with this bacteria has been shown to alleviate the burden of metabolic dysfunction 36 .

Study conclusion

This study supports the hypothesis that the gut microbiota are impacted by alcohol consumption…We conclude that gut microbes influence liver inflammation, neutrophil infiltration 37  and liver steatosis 38  following alcohol consumption and these data further emphasize the gut-liver axis, even in early alcohol-induced inflammation.

Discussion

The latter study seems to suggest that even relatively short-term heavy alcohol use can start the process of liver damage. The liver appears to be able to repair itself to some extent if alcohol consumption stops, but the latter process causes scarring of liver tissue that cannot be reversed. Over time, this reduces the amount of the liver that can function.

Alcohol consumption and pneumonia susceptibility

It’s not just the liver that becomes damaged when alcohol consumption causes gut dysbiosis. A June 2017 study 39 revealed how the natural defences of the heart and lungs against the bacteria that causes pneumonia (Klebsiella pneumoniae) are greatly weakened by excessive alcohol consumption. Once again, as with so many bodily reactions, this condition originates in changes to the gut microbiota.

Mice on a binge

The tests undertaken on mice showed that binge-drinking over a 48-hour period was sufficient to create a lung burden caused by an increased infection of the K. pneumoniae bacteria.

The following chart show the significant differences in specific symptoms of dysbiosis (intestinal fatty acid binding protein and and T-cells) between the pair-fed 40 control group and the alcohol-fed group:

Alcohol-dysbiosis significantly increases intestinal barrier damage and inflammation. (A) Circulating levels of intestinal fatty acid binding protein (i-FABP) in alcohol-dysbiosis and pair-fed recolonized mice. (B) Absolute number of effector (CD44+, CD62L-) CD8+ T-cells in the intestine of alcohol-dysbiosis and pair-fed recolonized mice. Bars are the mean ± SEM, *indicates P<0.05, by Mann-Whitney U. N = 10/group.

Discussion

The latter study once again emphasises the damage caused when the gut microbiota is altered through even short-term chronic alcohol consumption.

All alcohol in your drinks is ethanol

It’s easy to imagine that one drink is ‘safer’ than another – for instance, those who drink wine consider that it may be less harmful than beer, and those who drink beer might think it’s a healthier option than drinking spirits; however, the alcohol they each contain is the same thing – ethanol.

All chronic alcohol ingestion leads to bacterial overgrowth and dysbiosis in the small and large intestine of animals and humans 41 42 43 44 45 . Studies in mice have shown that ethanol reduces the bacteria phylum Firmicutes 46  and the genus Lactobacillus 44 , while the species Enterococcus 47 , Akkermansia, Corynebacterium, and Alcaligenes increase after alcohol administration 44 45 46 . Chronic ethanol consumption also markedly reduces amino acid metabolism, and perturbs the metabolism of steroid, lipid, carnitine 48 , and bile acid 49 . Additionally, after consuming ethanol, intestinal levels of short-chain fatty acids (SCFAs), as well as saturated long-chain fatty acids (LCFAs) are lower 50 51 .

Oral microbiota & alcohol

It’s not just the gut microbiota that gets damaged by alcohol, as was demonstrated in an April 2018 study 52 , the bacteria in our mouths also struggle to cope with ethanol intake.

A large number of human subjects were included in this study, and the researchers looked at the effects of all types of alcoholic drink (wine, beer and spirits) and also at different levels of consumption, from non-drinkers, through to infrequent and heavy drinkers.

Study results

They found that: “…alcohol consumption, and heavy drinking in particular, may influence the oral microbiome composition.” In particular, they found that alcohol consumption is associated with decreased abundance of Lactobacillales (‘good’ bacteria), and increased levels of the potentially pathogenic bacteria, Proteobacteria and Actinobacteria (‘bad’ bacteria). They considered that depletion of Lactobacillales, thought to be important for good oral health, may promote growth of other alkaline-tolerant bacteria 53 .

Mechanisms involved

Ethanol may indirectly increase certain bacterial taxa by decreasing Lactobacillales thereby increasing pH, as mentioned above, or by inhibiting the antimicrobial properties of saliva and by disturbing the host-microbial balance. Additionally, alcohol could impair neutrophil function (contributing to bacterial overgrowth and increased bacterial penetration), reduce monocyte production of inflammatory cytokines (allowing for microbial proliferation), and have adverse effects on teeth (stimulating bone resorption and suppressing bone formation) [and the periodontium.

Layers within a human tooth

Long- and short-term damage

Both acute (short-term) and chronic (long-term) ethanol exposure were considered by this study to lead to functional changes in saliva, including decreased flow rate and impaired output of total protein, amylase, and electrolytes.

Different types of alcoholic drink

Whilst the study found some differences between the oral microbiota of non-drinkers and wine drinkers – specifically, wine-drinkers had a richer and different microbial profile from non-drinkers, with a decreased abundance of the phyla Bacteroidetes and Firmicutes, the family Peptostreptococcaceae) – the study concluded that: “Because our study had limited numbers of subjects who exclusively consumed beer, wine, or liquor, further study is required to disentangle the differential effect of each type of alcoholic beverage on oral microbial composition.” They did, however, point out that any variations that may occur between different types of alcoholic drink, probably derive simply from the relative percentage of ethanol contained.

An article in NewsMedical.net 54  pointed out that some of the different species found in drinkers compared with non-drinkers included the species, Actinomyces, Leptotrichia, Cardiobacterium, and Neisseria. “These strains have been known to raise the risk of head and neck cancers as well as a cancers of the food pipe or esophagus and pancreas….heavy drinkers showed more pronounced presence of these bacteria. The bacteria interacted with the alcohol as it was broken down by the body and this led to preferential growth of certain strains of the bacteria. The strains of healthy bacteria Lactobacillales were however much reduced.

Discussion

It would be interesting to compare the effects of drinking 100% pure ethanol with lower percentages. It would be no surprise to me to find that the changes to microbiota, wherever we are looking within the body, would be to a large degree proportional to the percentage of ethanol consumed. Naturally, there would be some bacterial and other physiological changes caused by added ingredients (such as other chemicals from grapes, barley, hops, rye, etc) within each drink; but the effects of the ethanol may well be relatively consistent, depending on percentage of content.

Psychiatric disorders, alcohol and the microbiome

Alcohol, microbiome and neuroinflammation.

A July 2018 study 55 confirmed what we have already discussed in a previous blogs 3 4 , namely the essential role that the body’s microbiome plays in our psychological well-being. This particular study considered the growing body of evidence showing that alcohol consumption increases brain levels of certain molecules that signal to our body’s immune system that something is wrong, resulting in neuroinflammation. Similar results had already been found in studies on other animal models 56 .

Our central nervous system (CNS), which includes the brain and spinal cord, has certain immune responses when it senses danger. The researchers note that the microbiota play a pivotal role in this process and affect central neurochemistry and behaviour: “Disruption of or alterations in the intimate cross-talk between microbiome and brain may be a significant factor in many psychiatric disorders. Alterations in the composition of the microbiome, so called dysbiosis, may result in detrimental distortion of microbe-host homeostasis modulating the hypothalamic-pituitary-adrenal axis.” Heavy alcohol consumption can play a significant causal role in dysbiosis and, in turn, dysbiosis and psychiatric disorders appear to be strongly linked.

Psychiatric pathologies associated with these changes in the community structure and function of the gut microbiota, include irritable bowel syndrome (IBS), depression, anxiety disorders, schizophrenia, and alcoholism.”

Study conclusion

“…emerging data suggests that alcohol induced alterations of the microbiome may explain reward-seeking behaviors as well as anxiety, depression, and craving in withdrawal and increase the risk of developing psychiatric disorders.

Discussion

We probably all could have guessed that research would find alcohol can causes short- and long-term psychological changes; but maybe not so many of us knew that the trillions of bacteria within us are so intimately connected with this process.

Effects of just one alcoholic drink

We’ve mainly looked at chronic alcohol consumption, but when we looked above at the 2003 study 23 , we saw that even a single heavy drinking session (a so-called ‘binge’) can cause significant damage, including inducing a leaky gut. However, most of us would assume that negative psychological and psychological effects would be significantly less when we drink only a little alcohol infrequently.

10 symptoms of potential sensitivity to alcohol

Your gut may already be reacting (whether you are aware of it or not) to the quantities of alcohol you consume, if you:

  • find it hard to lose weight and/or gain weight easily
  • experience frequent constipation and/or diarrhoea
  • flush easily, particularly during/after consuming alcohol
  • suffer from acid reflux, ulcers, or other stomach acid problems
  • have food allergies, seasonal allergies, or histamine issues
  • have skin problems, for instance eczema, psoriasis, acne, or rashes
  • have a history of hormone problems
  • have an existing autoimmune disease, disorder, or other chronic health problem, including thyroid, adrenal, intestinal, digestive, or metabolic
  • have an GIT (gastro-intestinal tract) condition, for instance SIBO (small intestinal bacterial overgrowth), dysbiosis, leaky gut, or coeliac disease
  • have liver problems

The above is by no means meant to be a comprehensive list of possible associated conditions, nor is it meant to be a diagnosis; however, if you do drink alcohol and experience some of these effects, it might be worth taking a closer look at whether alcohol is playing a part.

Final thoughts

This has been a somewhat random and potted look at some of the studies relating to alcohol and the microbiota. For me, the take-home message is that consuming alcohol, in any form, is something we do because of its psychological effects (making us feel relaxed, giving us a buzz, allowing us to act with more confidence, or being able to forget our worries and feel temporarily less stressed).

However, I suspect that none of us would choose to put ethanol into our bodies if it had no effect at all on how we felt. Whilst this might seem an obvious point, it does have some significance. What if our bodies and minds were sufficiently healthy and strong that we didn’t need the effects that alcohol to ‘sustain’ or ‘refresh’ us? What if our diet and lifestyle continually fortified us, so that we could weather the usual stresses of life?

From my research and personal experience, eating the optimal diet, getting plenty of exercise, sleeping well, and finding mindful ways of sailing smoothly through the rough seas of daily life are four lifestyle options that link together and have the potential of providing that fortification. At the core of it, at least in my opinion, is a WFPB diet. It provides all the nutrients we need, while at the same time avoiding all the toxins and empty calories that come part-and-parcel with animal and processed foods. A WFPB diet also brings with it, the psychological benefits of knowing you are taking the most effective step in helping to protect the environment and to reduce animal suffering.

Finally, the very concept of a WFPB diet is that you eat whole plant foods. Alcohol, of course, is not a whole plant food. Thus, whether we choose to drink it or not, it’s worth remembering that a glass of wine, beer or our favourite spirit is, in effect, a processed food. This may not seem such a big issue, but a side-effect of the addictive nature of so many processed foods and drinks also applies to alcohol and, as such, they can easily replace optimally healthy foods and drinks.

It’s no coincidence that the things you crave most after a good drinking session are things like kebabs, crisps, cakes, sweets and not lentils, salad, apples and broccoli!


References

  1. No Amount of Alcohol Consumption is Safe []
  2. Brief explanation of the difference between ‘microbiota’ and ‘microbiome’. Microbiota refers to the 100’s of different species of microbes (bacteria, fungi etc), while microbiome refers to the complete set of genes within these microbes. []
  3. Obstructive Sleep Apnea (OSA) & Gut Microbiota [] []
  4. Gut Microbiota & Depression [] []
  5. Fibromyalgia, Probiotics & Gut Microbiota []
  6. Multiple Sclerosis (MS), Serotonin & Gut Microbiota []
  7. Two Types of Gut Bacteria: Plant Eaters’ & Meat Eaters’ []
  8. IBD / Crohn’s Disease / Ulcerative Colitis & WFPB Diet Part 5 of 5 []
  9. Urinary Microbiome & Psychological Issues in Women with Overactive Bladder []
  10. Oral Microbiota – Meat-Eaters & Plant-Eaters []
  11. The Best Source of Resveratrol. Video by Michael Greger M.D. FACLM April 2nd, 2018 Volume 41 []
  12. The human body is home of trillions of bacteria, viruses, fungi, and other tiny organisms. These organisms are known as microbes. []
  13. Am J Physiol Gastrointest Liver Physiol. 2012 May 1; Colonic microbiome is altered in alcoholism. Mutlu EA, Gillevet PM, Rangwala H, Sikaroodi M, Naqvi A, Engen PA, Kwasny M, Lau CK, Keshavarzian A. []
  14. Proteobacteria include a wide variety of pathogens, such as Escherichia, Salmonella, Vibrio, Helicobacter, Yersinia, Legionellales, etc. []
  15. Alcohol Res. 2015;37(2):223-36. The Gastrointestinal Microbiome: Alcohol Effects on the Composition of Intestinal Microbiota. Engen PA, Green SJ, Voigt RM, Forsyth CB, Keshavarzian A. []
  16. Wikipedia: Intestinal permeability. []
  17. Definition of endotoxemia: The presence of endotoxins in the blood, which, if derived from gram-negative rod-shaped bacteria, may cause haemorrhages, necrosis of the kidneys, and shock. []
  18. NHS: Probiotics. []
  19. Definition of synbiotic: The term synbiotic is used when a product contains both probiotics and prebiotics. Because the word alludes to synergism, this term tends to be used for products in which the prebiotic compound selectively favours the probiotic compound. []
  20. Metabolic pathways are a linked series of chemical reactions occurring within a cell. The reactants, products, and intermediates of an enzymatic reaction are known as metabolites, which are modified by a sequence of chemical reactions catalysed by enzymes. []
  21. Concerns about processed probiotics. []
  22. Culture Shock – Questioning the Efficacy and Safety of Probiotics. Michael Greger M.D. FACLM October 25th, 2017 Volume 38 []
  23. Best Pract Res Clin Gastroenterol. 2003 Aug;17(4):575-92. Effect of alcohol consumption on the gut. Bode C, Bode JC. [] []
  24. PLOS One: Acute Binge Drinking Increases Serum Endotoxin and Bacterial DNA Levels in Healthy Individuals. Shashi Bala , Miguel Marcos , Arijeet Gattu, Donna Catalano, Gyongyi Szabo. Published: May 14, 2014https://doi.org/10.1371/journal.pone.0096864. []
  25. Bacterial translocation is the passage of viable bacteria from the gastrointestinal (GI) tract to extraintestinal sites, such as the mesenteric lymph node complex (MLN), liver, spleen, kidney, and bloodstream. []
  26. Vishnudutt Purohit,a, J. Christian Bode,b Christiane Bode,b David A. Brenner,c Mashkoor A. Choudhry,d Frank Hamilton,e Y. James Kang,f Ali Keshavarzian,g Radhakrishna Rao,h R. Balfour Sartor,i Christine Swanson,j and Jerrold R. Turnerk. Alcohol, Intestinal Bacterial Growth, Intestinal Permeability to Endotoxin, and Medical Consequences. Alcohol. 2008 Aug; 42(5): 349–361. []
  27. Definition of endotoxin: a toxin present inside a bacterial cell that is released when it disintegrates. []
  28. Difference between epithelial and endothelial cells: Endothelial cells form the endothelium, a thin layer that coats the inner surface of blood vessels. The cells always lie attached to the vessel wall. The inner wall of the entire circulatory system is covered with endothelial cells. They act as an interface between the circulating blood and the vessel wall. The endothelium is one-cell-layer thick and also lies attached to the interior of the heart chambers.  On the other hand, epithelial cells form the epithelium. This covers the outside portion of the body (the three layers of skin or epidermis), and also coats all the internal organs – including the liver, stomach, intestine, lungs, urethra, urinary bladder, and other organs of the body. Thus, epithelial cells provide a protective coating to the surface of the body and its internal tissues. []
  29. Acetaldehyde is a product of alcohol metabolism which is more toxic than the alcohol itself. Acetaldehyde is created when the alcohol in the liver is broken down by an enzyme called alcohol dehydrogenase. The acetaldehyde is then attacked by another enzyme, acetaldehyde dehydrogenase, and another substance called glutathione, which contains high quantities of cysteine (a substance that is attracted to acetaldehyde). Together, the acetaldehyde dehydrogenase and the glutathione form the nontoxic acetate (a substance similar to vinegar). []
  30. “Intestinal REG3 Lectins Protect against Alcoholic Steatohepatitis by Reducing Mucosa-Associated Microbiota and Preventing Bacterial Translocation.” Wang et al., Cell Host & Microbe 19, 1–13. http://dx.doi.org/10.1016/j.chom.2016.01.003 []
  31. Scientific American February 2016: Drinking Causes Gut Microbe Imbalance Linked to Liver Disease []
  32. Definition of downregulation: Downregulation is the process by which a cell decreases the quantity of a cellular component, such as RNA or protein, in response to an external stimulus. []
  33. Bull-Otterson L, Feng W, Kirpich I, Wang Y, Qin X, Liu Y, et al. Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome and the effect of Lactobacillus rhamnosus GG treatment. PLoS One. 2013;8(1):e53028. Epub 2013/01/18. pmid:23326376 []
  34. PLOS One. Alcohol-related changes in the intestinal microbiome influence neutrophil infiltration, inflammation and steatosis in early alcoholic hepatitis in mice. Patrick P. Lowe , Benedek Gyongyosi , Abhishek Satishchandran, Arvin Iracheta-Vellve, Aditya Ambade, Karen Kodys, Donna Catalano, Doyle V. Ward, Gyongyi Szabo. Published: March 28, 2017https://doi.org/10.1371/journal.pone.0174544. []
  35. Wang L, Fouts DE, Starkel P, Hartmann P, Chen P, Llorente C, et al. Intestinal REG3 Lectins Protect against Alcoholic Steatohepatitis by Reducing Mucosa-Associated Microbiota and Preventing Bacterial Translocation. Cell Host Microbe. 2016;19(2):227–39. Epub 2016/02/13. pmid:26867181 []
  36. Everard A, Belzer C, Geurts L, Ouwerkerk JP, Druart C, Bindels LB, et al. Cross-talk between Akkermansia muciniphila and intestinal epithelium controls diet-induced obesity. Proc Natl Acad Sci U S A. 2013;110(22):9066–71. Epub 2013/05/15. pmid:23671105 []
  37. Definition of neutrophil infiltration: Neutrophils are important disease-fighting white blood cells. Neutrophil infiltration is the diffusion or accumulation of neutrophils in tissues or cells in response to a wide variety of substances released at the sites of inflammatory reactions. []
  38. Definition of liver steatosis: the infiltration of liver cells with fat, associated with disturbance of the metabolism by, for example, alcoholism, malnutrition, pregnancy, or drug therapy. []
  39. PLOS Pathogens: Alcohol-associated intestinal dysbiosis impairs pulmonary host defense against Klebsiella pneumoniae. Derrick R. Samuelson , Judd E. Shellito, Vincent J. Maffei, Eric D. Tague, Shawn R. Campagna, Eugene E. Blanchard, Meng Luo, Christopher M. Taylor, Martin J. J. Ronis, Patricia E. Molina, David A. Welsh. Published: June 12, 2017. https://doi.org/10.1371/journal.ppat.1006426 []
  40. Definition of Pair-feeding: This is a technique where the amount of food provided to a control group of mice is matched to that consumed by the experimental group, so as to determine the extent to which the effect of a treatment on body weight or body composition occurred independently of changes of energy intake. []
  41. Bode JC, Bode C, Heidelbach R, Durr HK, Martini GA. Jejunal microflora in patients with chronic alcohol abuse. Hepatogastroenterology. 1984;31(1):30–4. Epub 1984/02/01. pmid:6698486 []
  42. Casafont Morencos F, de las Heras Castano G, Martin Ramos L, Lopez Arias MJ, Ledesma F, Pons Romero F. Small bowel bacterial overgrowth in patients with alcoholic cirrhosis. Dig Dis Sci. 1996;41(3):552–6. Epub 1996/03/01. pmid:8617135. []
  43. Engen PA, Green SJ, Voigt RM, Forsyth CB, Keshavarzian A. The Gastrointestinal Microbiome: Alcohol Effects on the Composition of Intestinal Microbiota. Alcohol Res. 2015;37(2):223–36. Epub 2015/12/24. pmid:26695747; PubMed Central PMCID: PMCPMC4590619. []
  44. Hartmann P, Chen P, Wang HJ, Wang L, McCole DF, Brandl K, et al. Deficiency of intestinal mucin-2 ameliorates experimental alcoholic liver disease in mice. Hepatology. 2013;58(1):108–19. Epub 2013/02/15. pmid:23408358; PubMed Central PMCID: PMCPMC3695050. [] [] []
  45. Yan AW, Fouts DE, Brandl J, Starkel P, Torralba M, Schott E, et al. Enteric dysbiosis associated with a mouse model of alcoholic liver disease. Hepatology. 2011;53(1):96–105. Epub 2011/01/22. pmid:21254165; PubMed Central PMCID: PMCPMC3059122. [] []
  46. Bull-Otterson L, Feng W, Kirpich I, Wang Y, Qin X, Liu Y, et al. Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome and the effect of Lactobacillus rhamnosus GG treatment. PLoS One. 2013;8(1):e53028. Epub 2013/01/18. pmid:23326376; PubMed Central PMCID: PMCPMC3541399. [] []
  47. MCC C , NL L , CM F , JL G , D A , C G , et al. Comparing the effects of acute alcohol consumption in germ-free and conventional mice: the role of the gut microbiota. BMC Microbiology. 2014;14(1):240. pmid:25223989 []
  48. Xie G, Zhong W, Zheng X, Li Q, Qiu Y, Li H, et al. Chronic ethanol consumption alters mammalian gastrointestinal content metabolites. J Proteome Res. 2013;12(7):3297–306. Epub 2013/06/15. pmid:23763674. []
  49. Xie G, Zhong W, Li H, Li Q, Qiu Y, Zheng X, et al. Alteration of bile acid metabolism in the rat induced by chronic ethanol consumption. Faseb j. 2013;27(9):3583–93. Epub 2013/05/28. pmid:23709616; PubMed Central PMCID: PMCPMC3752538. []
  50. Chen P, Torralba M, Tan J, Embree M, Zengler K, Starkel P, et al. Supplementation of saturated long-chain fatty acids maintains intestinal eubiosis and reduces ethanol-induced liver injury in mice. Gastroenterology. 2015;148(1):203–14.e16. Epub 2014/09/23. pmid:25239591; PubMed Central PMCID: PMCPMC4274236. []
  51. Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM. Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition. J Nutr. 2004;134(4):904–12. Epub 2004/03/31. pmid:15051845. []
  52. Microbiome. 2018 Apr 24;6(1):59. doi: 10.1186/s40168-018-0448-x. Drinking alcohol is associated with variation in the human oral microbiome in a large study of American adults. Fan X, Peters BA, Jacobs EJ, Gapstur SM, Purdue MP, Freedman ND, Alekseyenko AV, Wu J, Yang L, Pei Z, Hayes RB, Ahn J. []
  53. Bull-Otterson L, Feng W, Kirpich I, Wang Y, Qin X, Liu Y, Gobejishvili L, Joshi-Barve S, Ayvaz T, Petrosino J, et al. Metagenomic analyses of alcohol induced pathogenic alterations in the intestinal microbiome and the effect of lactobacillus rhamnosus GG treatment. PLoS One. 2013;8(1):e53028. []
  54. NewsMedical.net April 2018: Alcohol damages microbiome in the mouth []
  55. Prog Neuropsychopharmacol Biol Psychiatry. 2018 Jul 13;85:105-115. Alcohol, microbiome, and their effect on psychiatric disorders. Hillemacher T, Bachmann O, Kahl KG, Frieling H. []
  56. Am J Pathol. 2006 Apr; 168(4): 1335–1344. Alcohol Abuse Enhances Neuroinflammation and Impairs Immune Responses in an Animal Model of Human Immunodeficiency Virus-1 Encephalitis. Raghava Potula, James Haorah, Bryan Knipe, Jessica Leibhart,*Jesse Chrastil, David Heilman, Huanyu Dou, Rindha Reddy, Anuja Ghorpade, and Yuri Persidsky. []

Should I Alkalise My Body?

Some foods are acidic and others and alkaline. There’s been quite a bit of concern in some areas of the media, and even in nutritional circles, about the need to put effort into alkalising your body. This is because it’s claimed that if don’t take action to stop our bodies from becoming acidic, then we become more prone to a wide range of diseases, including cancer. But how much of this is based on solid research and how much is based on thin air?

You need to supplement your diet?

The idea is that we should take great care to eat only alkaline-forming foods and to avoid all acid-forming foods. All well and good but, in addition to this, we’re encouraged to take alkalising supplements which can contain several alkalising compounds such as:

  • sodium bicarbonate (baking soda) – something to be pretty cautious about doing 1
  • potassium hydroxideditto 2
  • sodium hydroxideditto  3
  • lemon juice powder
  • inulin
  • potassium citrate
  • calcium citrate
  • magnesium citrate
  • bamboo powder
  • cherry powder
  • the list goes on…
Just a handful of the wide range of (often v. expensive) alkalising supplements on the market.

The pH scale

Acidity and alkalinity are measured using the pH scale, which runs from 0 to 14.

  • 0 is very acidic
  • 7 is neutral
  • 14 is very alkaline

We’ve already looked at some of the benefits that research has uncovered about eating a largely alkaline diet 4 5 , but this has been in relation to eating a WFPB diet, and not taking questionable supplements or trying to raise alkalinity levels in an aggressive manner. But what’s wrong with trying to raise alkalinity throughout our bodies?

Our bodies have ‘compartments’

Different parts (or compartments) of our bodies have different natural pH levels. For instance:

  • stomach – pH of around 2 at rest and between 4 or 5 after a meal
    • amongst other negative effects, forcing the stomach to become more alkaline has been shown 6 to result in less iron absorption from our food
  • intestines – there are naturally varying pH levels (shown to be essential for health of our gut microbiome 7 ):
    • duodenum – pH of around 6
    • ileum – pH of around 7.4
    • caecum – pH of around 5.7
    • rectum – pH of around 6.7

  • vagina – pH of around 4.5  (lactic acid-secreting bacteria have been shown to be essential to prevent infections such as Candida albicans (thrush), which would develop in a neutral to alkaline environment) 8 9

And since the above is just a sample of the different pH levels required throughout the body, it should be clear that it may be unwise to try to ‘force’ alkalinity throughout the system.

Indeed, it’s not just a matter of being unwise to do so, it can be fatal.

The average pH level of our blood is strictly controlled so that it remains between a pH of 7.35 and 7.45, and our bodies have various complex and powerful mechanisms to ensure that this pH homeostasis is maintained.

However, if something overwhelms the ability of these ‘buffering’ mechanisms to do their job (such as introducing powerful alkalising supplements into your body or eating ), so that the blood pH rises above 7.7 (too alkaline), there’s one simple outcome – death. The same applies if unfortunate consequence occurs if blood pH drops below 7 (too acidic).

WFPB and pH level

So, how do we go about ensuring that our body is maintained at the optimal pH level?

We don’t. But our bodies do – if, that is, we eat an appropriate diet.

All animal products (including red/white meat, offal, fish, seafood, dairy – including cheese of course) and most processed foods have been shown to be acidic 10 while whole plant foods are mainly neutral to alkaline 11 . A WFPB diet, consisting largely of vegetables, fruits, legumes and whole grains is rich in fibre and resistant starch which ensure the gut microbiome have sufficient carbohydrate to make the short chain fatty acids which help maintain optimal pH in the colon. And you don’t need any of those expensive alkaline potions or pills to achieve this.

By eating a WFPB diet, you don’t have to think of yourself as “alkalising your blood”. Some plant foods are naturally more acidic/neutral/alkaline than others, but by eating a WFPB diet (particularly one without added salt, sugar or oil) , which is naturally balanced, you take the load off all the bodily mechanisms which would have otherwise have to work harder to maintain optimal pH should your diet consist of high acid-forming foods.

Kidney disease and pH level

There are huge and varied health benefits from eating a WFPB diet, and one of the clear benefits has been shown to be that the risk of kidney disease is greatly reduced, as compared with eating a diet rich in processed and animal foods 12 .

Final thoughts

As with so many aspects of human health, the simplest solutions are often the best. A non-SOS WFPB diet obviates the need for so many things that the media and even traditional nutritionists obsess about – such as protein-combining or calorie-counting. The same applies here: just eat the optimal diet and your body will maintain optimal pH level and hence optimal health – allowing you to find other things to worry about…


References

  1. Are Acid-Blocking Drugs Safe? Michael Greger M.D. FACLM October 29th, 2018 Volume 44 []
  2. NJH Hazardous Substance Fact Sheet – Potassium Hydroxide []
  3. ATSFR – Toxic Substance Portal – Sodium Hydroxide []
  4. Alkaline Diet – So What?! []
  5. Psoriasis & Eczema Cured by Alkaline Diet? Caution: Some Graphic Images []
  6. Gut. 1969 Mar;10(3):226-9. Role of gastric secretion in iron absorption. Jacobs A, Miles PM. []
  7. Fallingborg, J. (1999). Intraluminal pH of the human gastrointestinal tract. Danish Medical Bulletin, 46(3), 183-196. []
  8. Miller, E., Beasley, D., Dunn, R., & Archie, E. (2016). Lactobacilli dominance and vaginal pH: Why is the human vaginal microbiome unique? Frontiers in Microbiology, 7, 1936. []
  9. Vylkova, S., Carman, A., Danhof, H., Collette, J., Zhou, H., & Lorenz, M. (2011). The fungal pathogen Candida albicans autoinduces hyphal morphogenesis by raising extracellular pH. mBio, 3(e00055-11), 2. []
  10. Dr McDougall’s Nov 2003 Newsletter: How to Help a Meathead []
  11. Nutritionfacts: Alkaline Diet. []
  12. Mirmiran, P., Yuzbashian, E., & Bahadoran, Z. A. (2016). Dietary acid-base load and risk of chronic kidney disease in adults: Tehran Lipid and Glucose Study. Iranian Journal of Kidney Diseases, 3(119-125), 10. []

Having Pets in Childhood Predicts Dietary Choices in Adulthood

2018 study 1 looked into the association between choosing to eat a plant-based diet as an adult and having had pets as a child.

Previous studies 2 3 4  have shown that having pets as a child is a good predictor of the the likelihood that you will adhere to some sort of plant-based diet in adulthood.

Quantity matters when it comes to pets

So, taking this previous research into account, this study wanted to test the hypothesis that the number of different types of pets owned in childhood is positively associated with a reduction of animal consumption in adulthood.

Within the people covered in the study, the number of different types of pets owned in childhood ranged from 0 to 6.

Study results

They found that individuals who grew up around a greater variety of pets (i.e., hamsters, dogs, birds, and cats, as opposed to any number of dogs alone) were more likely to engage in greater degrees of meat avoidance (i.e., vegan as opposed to semi-vegetarian) in adulthood.

Those children who had a greater number and variety of pets as children were significantly more likely to end up as vegans as adults.

The researchers concluded: “Findings support the hypothesis that individuals who owned a greater variety of pets in childhood endorse more concerns regarding animal use. This, in turn, appears to predict the decision to refrain from animal products in adulthood.

Final thoughts

I suppose most of us would have predicted the above outcome, although it was interesting to see that greater number and variety of childhood pets is strongly associated with greater meat avoidance in adulthood. This all seems to be linked to a  ‘circle of compassion‘, as the study says, although this compassion does not necessarily have to mean that, as a child, you had a ‘cuddly’ relationship with the pets. For instance, having childhood pets such as horses, sheep, goats , snakes, hedgehogs, etc (with which you would be unlikely to have the sort of intimate relationship expected from a dog or cat), was still a strong predictor of meat avoidance in adulthood.

Whilst my main concern for promoting a WFPB diet is linked to its benefit for human health, there is a direct link with benefits for all other species on this small blue planet, as well as the planet itself.

So it may be claimed that making the decision to go plant-based could, in the long-run, be a win-win for all concerned.


References

  1. Appetite. 2018 Apr 1;123:43-48. doi: 10.1016/j.appet.2017.12.005. Epub 2017 Dec 7. Ethical concerns regarding animal use mediate the relationship between variety of pets owned in childhood and vegetarianism in adulthood. Heiss S, Hormes JM. []
  2. Paul, E. S., & Serpell, J. (1993). Childhood pet keeping and humane attitudes in young adulthood. Animal Welfare, 2, 321e337 []
  3. Paul, E. S., & Serpell, J. (1994). Pets and the development of positive attitudes to animals. In A. Manning, & J. Serpell (Eds.), Animal and human Society: Changing perspectives (pp. 127e144). New York, NY: Routledge. []
  4. Rothgerber, H., & Mican, F. (2014). Childhood pet ownership, attachment to pets, and subsequent meat avoidance. The mediating role of empathy toward animals. Appetite, 79, 11e17. []

Are Energy Drinks Harmful?

Our bodies operate optimally when we consume natural whole foods. This is why the WFPB diet is the optimal diet. However, energy drinks, such as Red Bull  and Monster are far from being a healthy whole food; but does this mean their only problem is that they fail to be optimally healthy? It could be that it’s far worse than that – one of their effects is potentially fatal.

A 2017 randomised, double-blind, controlled, cross-over trial 1 compared the effects of drinking high energy drinks and drinking caffeine on its own on a group of young healthy individuals.

ECG and blood pressure readings were taken at intervals after consumption.

As suspected, caffeine on its own (blue line on graph below) raised blood pressure within an hour, but pressure soon dropped thereafter.

However, the energy drink (red line on graph below) raised blood pressure at a later stage and in a way that caused some alarm.

The reason for the concern was that the energy drink (and not caffeine on its own) caused something called a ‘prolonged QT interval‘.

What’s a QT interval?

When you have an ECG 2 (also known as an EKG), there are a number of heart beat peaks and troughs on the resulting readout, as can be seen from the following (courtesy of Dr Greger’s video 3 regarding this subject):

QT Interval shown on typical ECG readout

The QT interval is the distance from the start of the downward Q wave to the end of the bump of the T wave.

As the study reports, if this QT interval is increased by more than 60 milliseconds (ms), then this is a “…recognized marker of increased risk for fatal arrhythmias.” 

The results from this study showed that energy drink consumption (a 946 mL or 32 ounce can) caused an increase in QT prolongation of around 10 ms in these young participants.

This might not see much, but it strikes home when you realise that some pharmaceuticals which raised the QT interval by as little as 5 ms (such as Cisapride 4 and Ephedra-containing drugs 5 ) were withdrawn from the market because of concerns about public health.

Energy drinks and obesity

The authors point out that this is particularly the case for anyone who is overweight or obese, since at least one study 4 showed an elevated risk of QT prolongation in the latter individuals, even when they consumed relatively small quantities of energy drinks.

What’s in energy drinks?

We know that caffeine is generally included, along with stuff like ginseng 6taurine 7 , carnitine 8 , guarana 9  etc, all of which in supplement form are things to consider carefully before being persuaded to take; but it may be the combination of these and other ingredients that can cause added problems. The body is an incredibly complex system which is continually affected by the the quantity, quality and combination of elements that we put into it.

Regulation of energy drinks

Because these drinks are mostly consumed by younger people, often along with alcohol, there are increasing concerns by medical and government bodies about whether there should be more regulation about their easy availability. Several studies have pointed out similar and additional problems as the above study has highlighted, with a request for more research to be done about their potential harms 10 11  .

Final thoughts

Repeated and heavy use of energy drinks is probably not a good idea. It’s not just that they contain isolated ingredients, something which a WFPB diet ideally avoids, but also because the ingredients are in combination with each other, and this can cause a complex of effects on the body which could result in both short- and long-term harm.

Additionally, very little research has been undertaken on other groups of energy drink consumers, apart from the healthy young adults in the above study, such as those with existing health issues (high blood pressure, heart/liver/kidney disease, etc) and both younger and older individuals.

Since energy drinks are unregulated, there’s no guarantee of what might have been added in order to give the consumer a ‘buzz’.  For instance, in 2008, Red Bull was forced to remove cocaine from its drinks 10 .

Finally, if you need something to raise your energy levels or give you a buzz, whether it’s via tobacco, alcohol, cocaine or energy drinks, then it’s likely that your health is already in deficit. If you eat a WFPB diet, exercise regularly, get enough quality sleep, and learn to avoid stress from affecting you too badly (e.g through mindfulness), then you should have all the energy and zest for life that  you need.

    Some potential effects of energy drink consumption.

References

  1. J Am Heart Assoc. 2017 Apr 26;6(5). Randomized Controlled Trial of High-Volume Energy Drink Versus Caffeine Consumption on ECG and Hemodynamic Parameters. Fletcher EA, Lacey CS, Aaron M, Kolasa M, Occiano A, Shah SA. []
  2. Definition of ECG/EKG/Electrocardiography []
  3. Are There Risks to Energy Drinks? Michael Greger M.D. FACLM October 24th, 2018 Volume 44. []
  4. Roden DM. Drug‐induced prolongation of the QT interval. N Engl J Med. 2004;350:1013–1022. [] []
  5. McBride BF, Karapanos AK, Krudysz A, Kluger J, Coleman CI, White CM. Electrocardiographic and hemodynamic effects of a multicomponent dietary supplement containing ephedra and caffeine: a randomized controlled trial. JAMA. 2004;291:216–221. []
  6. Ginseng supplements []
  7. Taurine supplements []
  8. Carnitine supplements []
  9. Guarana supplements []
  10. Pediatrics. 2011 Mar;127(3):511-28. doi: 10.1542/peds.2009-3592. Epub 2011 Feb 14. Health effects of energy drinks on children, adolescents, and young adults. Seifert SM, Schaechter JL, Hershorin ER, Lipshultz SE. [] []
  11. Postgrad Med. 2015 Apr;127(3):308-22. doi: 10.1080/00325481.2015.1001712. Epub 2015 Jan 6. Energy drinks and their adverse health effects: A systematic review of the current evidence. Ali F Rehman H, Babayan Z, Stapleton D, Joshi DD. []

HbA1c & Plant-Based Diets (Warning – Disturbing Images)

Hands up if you don’t know what HbA1c is? Very honest of you… For those us who need reminding, it’s simply a blood test to see what your average blood glucose (sugar) levels have been for the past two to three months. If you have a high HbA1c, it means you’ve got too much sugar in your blood. So what? Well, you’re then likely to develop diabetes complications. So, if you want to avoid nasty stuff, such as blindness, limb amputation and increased risk of heart disease, can a plant-based diet help?

High or low is best?

High levels of HbA1c are not what you want. You want to have results that show that you’re blood sugar levels over the past 2-3 months have been low – that’s a sign that you’re not heading towards diabetes and all the accompanying horrors and inconveniences that this completely avoidable disease brings with it.

The horrors of diabetes – amputation,
The Horrors of diabetes – blindness

A recently published study 1 is a response to the fact that diabetes is now a major public health concern around the world – with around 180 million known cases and every indication of the numbers increasing hugely over the next decades 2 .

Study background

Previous blogs 3 have already considered the evidence that a plant-based diet can reverse diabetes mellitus (also known as Type 2 Diabetes) in a way that no current pharmaceutical or surgical method can even approach – and we’ve known this for many decades. But this is the first study to critically appraise whether plant-based diet reduces the HbA1c level compared to conventional diet.

Study method

The researchers reviewed and appraised relevant previous literature on this subject in order to evaluate whether or not there was sufficient evidence to suggest that HbA1c would be reduced in a plant-based diet group compared to a conventional diet group.

Study results

At a 22 weeks follow-up of both groups, they found that there was a significant reduction in HbA1c levels in the plant-based group compared with the conventional diet group. And the results were not temporary.

At a 72 week follow-up, they found that the plant-based diet group once again showed significant reduction in HbA1c compared with the conventional diet group.

Study conclusion

The authors’ conclusion was no surprise: “In patients with type 2 diabetes mellitus, changing to a plant-based diet reduced HbA1c levels compared with patients with conventional diet.

Final thoughts

You can get home test kits for your HbA1c levels 4 , or get simple finger-prick tests that looks at a wide range of additional health indicators (such as cholesterol and vitamin/mineral levels, organ health, anaemia, fatty acid concentrations etc) which you then send off to a laboratory and get an email with a detailed report and doctor’s comment. I use Medichecks 5 myself.

Your health is in your hands TODAY. Don’t wait for obvious symptoms of disease before switching to a WFPB diet. The only side-effect you’ll experience is improved health, vitality and life-span. A win-win situation for your health and the health of the planet 6 .


References

  1. Acta Med Indones. 2018 Jul;50(3):260-267. Plant-based Diet for HbA1c Reduction in Type 2 Diabetes Mellitus: an Evidence-based Case Report. Utami DB, Findyartini A. []
  2. Vegetarian Diets and the Risk of Diabetes []
  3. Diet Reverses Type 2 Diabetes – How Long Have We Known This? []
  4. Home test kit for HbA1c levels. []
  5. Medichecks simple blood tests. []
  6. A Sustainable Diet for Our Planet []

NHS Cuts Out Sugar

 

A recent NHS report entitled ‘Every NHS hospital in England to cut sugary drinks sales‘ 1 has agreed to cut their sales of sugary drinks on their premises. The NHS England says that it’s all part of their action to tackle the rising levels of obesity in the nation. But is it too little, too late?

Total ban?

Not at all. The 227 NHS Trusts are simply pledging to reduce sales of sugar-sweetened drinks to 10% or less of their total drinks sales.

There’s no indication of exactly when they are pledging to do this. We hear lots of pledges – usually from politicians who then either forget they made the pledges or adjust the pledge to mean something different from what was first stated.

Hopeful signs

23 NHS Trusts and two retailers have decided to stop selling sugary drinks altogether.

There is no clear indication of what ‘sugary drinks’ means here.

The NHS report states that sugar-sweetened drinks sold on NHS premises has reduced for seven months in a row falling to just 7.4% in participating Trusts in June 2018.

NHS comment

Simon Stevens, Chief Executive of NHS England said:

Every hospital in the country is now answering this important call to action and the NHS is rightly leading the way in battling the growing obesity epidemic across the country.”

I think it’s a bit of an overstatement to claim that the NHS is leading the way. Have you seen the sort of food they give patients? And even allowing the likes of Costa Coffee and Greggs inside their premises is far from the standards set by anyone eating a WFPB diet, since there’s hardly anything at all you could eat or drink that Costa or Greggs sell.

If, however, they mean that they are leading the way when compared with other national health authorities, then of course they’re going to lead – they are the only one in England!

Retailers inside NHS premises

14 retailers which operate inside NHS premises (including WH Smith, Boots, Marks & Spencer and Greggs), have signed up to this modest NHS ‘health drive’.

NHS staff – credible health workers?

It’s pretty shocking to hear NHS’s own figures that, of their 1.3 million plus staff in England alone, nearly 700,000 of these are estimated to be overweight or obese. This is not a surprise when you visit hospitals. Their staff look more unwell than many of the patients – especially when they’re lounging against the outside walls with a fag in one hand and a can of Coke in the other.

Final thoughts

It could be viewed as tokenism if they are simply targeting ‘added sugar’ drinks. This is because many soft drinks contain artificial sweeteners, and these have been shown 2 to be as bad as, or even potentially worse than, sucrose for human health.

I applaud any efforts to address the catastrophe that our current national dietary and health policies are causing on the health of our people. But this will be too little too late for some many people who have already developed the unhealthy dietary habits, which are really tough to break, and who have already inflicted possibly irredeemable damage to their bodies and their prospects of long and healthy lives.

And what about the real culprits – high-fat, processed animal foods? I guess it’s just too much for the NHS to try and tackle Big Food, especially when most of the NHS committees will consist of people who actually eat this junk – even when they are at work…

When you visit an NHS hospital you may have seen the corridors-full of obese and over-weight NHS staff, and it may have occurred to you that, for the majority of these unfortunate carers, their patients are simply keeping the beds warm for them.


References

  1. NHS England: Every NHS hospital in England to cut sugary drinks sales []
  2. Bitter Effects of Artificial Sweeteners []

Middlesbrough – Parmo Heaven…Chronic Illness Hell

We’ve already covered the obesity crisis in the North East of England 1 , but I couldn’t resist sharing an article with you which just appeared in i News, entitled “The problem with the nation’s health isn’t the parmo – it’s what it represents.” 2 .

What’s a parmo?

If you don’t come from Teesside, you’re unlikely to know what a parmo is. It’s something that appears to be quite unique to this area – certainly in terms of its established popularity as part of an utterly unbalanced diet.

It consists of either a breaded chicken or pork escalope, deep fried and topped with a bechamel sauce and some form of greasy high-fat cheese (Parmesan or Cheddar usually).

They come in at around 2,000 calories a serving (more than most non-athletic adults should consume in a whole day) and are usually accompanied with a massive pile of fried chips (French fries to those outside of the UK) and a can of Coke or Irn Brew, being that we’re “up North”.

Parmo history

The parmo was apparently brought to the Boro over 70 years ago by some American soldier after WWII.

Parmo availability

The Asda chain, owned now by Wal Mart, has a store in Stockton, next to Middlesbrough. It’s the only one of there 600+ UK stores to stock the parmo. Any coincidence that life expectancy in the poorer parts of Teesside are as low as 47 years of age – 18 years less than in more affluent areas 3 4 ?

Good old Asda – always worth a visit if you want to avoid eating too healthily…

Parmo madness

Tees Valley, which includes Middlesbrough, has a mayor called Ben Houchen. Believe it or not, he’s been campaigning 5 to get the parmo a Protected Designation of Origin Status from the EU, the same as Champagne, Melton Mowbray pork pies and Cheddar cheese have.

Great to see such concern for locals’ health from our local government…

A bit of parmo-related research

A March 2018 UK Government research document 6 pointed out that:

In 2015/16, bariatric surgery after a diagnosis of obesity was most common in North East England, where one in eight surgeries were performed. By comparison, one in every 21 people in England live in the North East.

Another report, just released by the NHS 7 , pointed out that 10-year-old children in the North-East were ranked as the most unhealthy in Britain. 23 percent of them are classified as obese.

Pretty shocking figures, but I’m actually surprised it’s such a low figure when I see children in the town centre. There are some (e.g. Dr Joel Fuhrman 8 ) who argue that the classification of obesity should be lowered from a BMI above 25 to above 23. This is because of the changes in health status once BMI passes 23.

And Tam Fry, chairman of the National Obesity Forum is quoted as saying, when asked where the blame lies for the North East’s horrendous obesity statistics: ““I can answer in two syllables…Parmo.

Tam Fry, Chairman of the National Obesity Forum

WFPB or not?

You can usually tell whether or not a person eats a WFPB diet from looking at their belly!

The ideal answer to the health problems caused by artery-clogging frankenfoods like parmos is so simple and yet so difficult for most people to consider possible – eat non-processed plant foods. It’s as simple as that.

Of course, neither local government in the areas affected nor national government are likely to start suggesting anything so extreme as eating the optimal diet for human health; but at least they can ensure that the NHS and doctors surgeries can get more funding so that they can cut more people open to repair their ravished bodies and stuff them with more pills to reduce some of their unnecessary suffering and pain.

What a world we live in…

Final thoughts

An interesting point raised by the iNews article is that people in the poorer parts of mainland Europe have tended to eat more healthy, locally produced food as a necessity, and not a luxury. However, “In Britain, unfortunately, it’s something of a race to the bottom: load it up and sell it cheap. The parmo is not the problem in itself. It is more the symbol of a careless attitude to nutrition that extends way beyond the North-East.” Can’t argue with that.


References

  1. Get Rich or Die Young? It’s the Food! []
  2. i News: The problem with the nation’s health isn’t the parmo – it’s what it represents. []
  3. “Knowingly and Secretly Deciding to Put the Buying Public at Risk” []
  4. Dying young in Stockton – England’s most unequal town []
  5. ‘Is it an appropriate use of time and effort?’: Mayor’s bid to protect the parmo under fire []
  6. BRIEFING PAPER Number 3336, 20 March 2018. Obesity Statistics []
  7. NHS Obesity News []
  8. Excess weight does not protect against heart disease []

A Sustainable Diet for Our Planet

An October 2018 study 1 entitled “Health and nutritional aspects of sustainable diet strategies and their association with environmental impacts: a global modelling analysis with country-level detail” has just been published in the Lancet. Will the findings show that there is any health/environmental benefit if populations around the world transitioned from an animal-based to a plant-based diet? Let’s find out…

Study background

There are considerable concerns about the negative impact that current trends in food production and consumption are having on human health and the environment we live in – including, of course, all the other species that share this planet with us. Thus, there’s increasing pressure to find sustainable diets that can address these issues.

This study looks at more than 150 countries, and examines the following four different diets:

  • flexitarian
    • no processed meat, small amounts of red meat (one serving per week), moderate amounts of other animal-source foods (poultry, fish, and dairy), and generous amounts of plant-based foods (fruits, vegetables, legumes, and nuts)
  • pescatarian
    • meat replaced with two-thirds fish and seafood and a third fruits and vegetables
  • vegetarian
    • meat replaced with two-thirds legumes and a third fruits and vegetables
  • vegan
    • all animal-source foods replaced with two-thirds legumes and a third fruits and vegetables

Study methods

To produce the wide-reaching global model they required, the researchers combined analyses of:

  • nutrient levels
  • diet-related chronic disease mortality
  • weight-related chronic disease mortality
  • general environmental impacts

They focused on three major objectives:

  • environmental
    • replacing 25-100% of animal-source foods with plant-based foods
  • food security
    • reducing levels of underweight, overweight, and obesity by 25-100%
  • public health
    • analysing the above-mentioned four dietary patterns (flexitarian, pescatarian, vegetarian, and vegan)

Their analyses took into account:

  • required nutrient content and sufficiency of supply
  • changes in mortality based on predicted changes in diet- and weight-related risk
  • country-specific and food group-specific footprints for:
    • greenhouse gas emissions
    • cropland use
    • freshwater use
    • nitrogen application
    • phosphorus application

These would help to analyse the relationship between the health and environmental impacts of any given dietary change.

Study findings

Replacing animal-sourced foods with plant-based ones was predicted to result in the following:

  • there would be an improvement in nutrient levels, particularly in high-income countries
  • premature mortality would be greatly reduced (more for a vegan than for a flexitarian diet)
  • a range of environmental impacts would reduce
    • for instance, greenhouse gas emissions could be reduced by up to 84%
  • freshwater use would:
    • increase by up to 16% if everyone ate a completely meat-free diet
    • reduce by 2-11% if meat-consumption was reduced greatly where it was energy-efficient to do so
  • nitrogen application could reduce by 23-25%
  • phosphorus application could reduce by 18-21%
  • cropland use could reduce by 8-11%
  • freshwater use could reduce by 2-11%

Study conclusion

A public health strategy focused on improving energy balance and dietary changes towards predominantly plant-based diets that are in line with evidence on healthy eating is a suitable approach for sustainable diets.

Final thoughts

Whilst this extensive study came up with the sort of conclusion most of us would expect, there are a few anomalies.

Firstly, the researchers consider that a meat-reduced diet would reduce greenhouse gases slightly more than a completely meat-free diet. I think this might in part be due to an increased need for transportation of plant-foods to areas where growing plants was not possible.

Secondly, the increased use of freshwater for completely meat-free diets, compared with largely meat-free diets where it is energy-efficient to do so, might be because eating fish and crustacea, where they are easily available, is more efficient than planting crops or having crops transported to the population concerned. This may also apply to areas where hunting wild animals, rather than planting crops, would have some energy-saving benefit.

Thirdly, in this study, there appears to be little recognition of the many negative effects of a meat-based diet on human health (and, of course, on the health of other species, not least the animals that act as our food). The harms to human health that animal foods produce, and which plant foods do not, is not mentioned in this study.

The authors’ final words are: “Finding effective combinations of policies and approaches that consider local characteristics will be essential for successfully upscaling initiatives and achieving reductions in the health and environmental burden at the population level and globally.

This may be taking into account those places where it is either impossible or impractical to grow crops 2 compared with either eating sea food, hunting wild animals or keeping some form of livestock that can exist on land that humans could not cultivate. This may account for the above findings related to the greater freshwater usage and slightly lower reductions in greenhouse gases if everyone adopted a completely meat-free diet.


References

  1. Lancet Planet Health. 2018 Oct;2(10):e451-e461. doi: 10.1016/S2542-5196(18)30206-7.
    Health and nutritional aspects of sustainable diet strategies and their association with environmental impacts: a global modelling analysis with country-level detail. Springmann M, Wiebe K, Mason-D’Croz D, Sulser TB, Rayner M, Scarborough P. []
  2. The main physical factors that make agriculture possible or impossible are: Climate. Some crops grow better in one climatic zone than in others. In general, plants cannot grow in areas with very high temperatures (above 45°C) or very low ones (below 10°C). They cannot grow in areas with too little rain or too much rain. Landscape. Relief (altitude and the gradient of terrain) influences agricultural activity. At higher altitudes, temperatures descend, and this limits species development. Gradients of terrain above 10° make it impossible to cultivate the land. Consequently, agriculture usually takes place on plains or in valleys. However, where it is necessary, hard work can transform mountain sides into cultivated terraces. Soil. Plants need soil with certain characteristics. The grain size and porosity of the soil affect the amount of oxygen the soil contains, and its ability to retain water. The chemical and biological composition of soil determines its degree of acidity, the quantity of mineral nutrients, and available organic matter. []

Eating Fruit Between Meals – Bad News for Teeth?

For a long time, studies 1 2   have shown that drinking sugary carbonated drinks causes tooth wear (where the enamel breaks down and the underlying dentine becomes exposed). However, (A) what about eating fruit, a central part of the WFPB diet, with meals and between meals and (B) what about cleaning teeth immediately after eating fruit – protective or destructive of that essential dental enamel layer?

A 2017 study 3 looked at both questions, (A) and (B), and came up with some interesting findings.

Study method

This was a case-controlled study that looked at 600 individuals who answered a detailed questionnaire and were then closely questioned by the researchers about their habits in relation to timing and frequency of both fruit consumption and teeth cleaning. They also analysed their consumption of acidic beverages, such as carbonated sugary soft drinks (Coke etc) and fruit juices.

Study findings

Unsurprisingly, they found that there was a strong association between tooth wear and drinking acidic beverages, whether or not they were consumed with or between meals.

They also found that there was no apparent relationship between tooth wear and eating fruit with a meal.

However, they found that there was a significant increase in tooth wear for those who regularly eat fruit between meals.

A bit of a surprise, since having fruit as a snack is a central part of so many people’s healthy diets.

Finally, they concluded that there was no significant relationship between tooth wear and cleaning teeth within 10 minutes of fruit consumption.

This, again, was a bit of a surprise since the conventional thinking has been that we should leave at least half an hour between consuming fruit (or any acid-forming food/beverage) and cleaning teeth, largely because it’s thought the former ‘softens‘ the latter for a short period of time, and so it’s best to wait for the enamel to ‘re-harden’ before brushing.

Discussion

Children and soft drinks

The UK Child Dental Health Survey of 1993 4 revealed that dental erosion was a problem in children, with acidic dietary components (foods and drinks) thought to be the main causal factors.

Following on from this, a May 2000 study 5 found that children with most dental erosion drank acidic beverages a lot more frequently than children without such erosion. They also drank significantly less milk and water, and were more likely to have a ‘swishing‘ or holding habit associated with drinking – holding the acidic drink in the mouth for longer.

This latter study also found that fruit and vinegar consumption had a stronger link with dental erosion. Interestingly, this association was also found for those who regularly took vitamin C supplements.

What about cavities?

A Feb 2004 study 6 confuses the picture a little by pointing out that dental caries (cavities) are less common in those who consume more fruit, whilst still agreeing with the above studies that consumption of soft drinks (which contain high levels of highly-acidic sugar) is a major cause of caries. This study did not look at erosion of the enamel due to fruit/soft drink consumption.

Saliva and tooth erosion

A 2006 study 7 agrees with the probable mechanism involved in the 2017 study’s 3 finding that eating fruit with a meal doesn’t cause any apparent dental erosion:

It’s the saliva!

The 2006 study researchers found this out by doing tests with chewing gum, as a means of replicating what happens when one eats fruit with a meal. They found that there’s less enamel wear if chewing gum is chewed after exposing the teeth, in this case, to a sugary soft drink. They concludes that: “salivary stimulation after an erosive or erosive/abrasive attack can reduce the dental wear...”

Final thoughts

All the above studies point to the fact that more research is needed – both clinical and epidemiological – to answer question (A) mentioned in the first paragraph above.

However, for the time being, it would seem that a sensible step is to chew gum (sugar-free, of course) immediately after eating fruit if consumed between meals, and to eat fruit with your regular meals. I try to have at least 7-9 servings of fruit and berries every day, mixing them with morning muesli, incorporating them into salads, and eating them as desserts with some nuts and seeds.

Regarding question (B), it appears that current research findings still leaves us somewhat in the dark about whether or not we should wait 20-30 mins after eating fruit before we clean our teeth. Once more research is published on this, I’ll let you know.

In the meantime, flossing immediately after eating any food is really important, as is drinking fluids (ideally water or tea) after meals, probably incorporating a bit of that ‘swishing‘ mentioned above to reduce any potential wear that the fruit acids might cause.

Finally, whilst there are some concerns about dental erosion and fruit consumption, remember that the research shows those who eat more fruit have less dental cavities.

This is not a blog to encourage us to eat less fruit – rather, if anything, most of us need to eat more fruit, but just ensure that we keep up-to-date with research to ensure we know how best to minimise any potential dental erosion.

Nothing in life is ever as simple as it first seems…


References

  1. Community Dent Health. 1997 Sep;14(3):143-7. Risk factors associated with tooth wear in teenagers: a case control study. Milosevic A, Lennon MA, Fear SC. []
  2. R. Moazzez, B.G. Smith, D.W. Bartlett, Oral pH and drinking habit during ingestion of a carbonated drink in a group of adolescents with dental erosion., J. Dent. 28 (2000) 395–397. []
  3. J Dent. 2017 Jan;56:99-104. doi: 10.1016/j.jdent.2016.11.005. Epub 2016 Nov 14. Timing of dietary acid intake and erosive tooth wear: A case-control study. O’Toole S, Bernabé E, Moazzez R, Bartlett D. [] []
  4. Children’s dental health in the United Kingdom, 1993 : a survey carried out by the Social Survey Division of OPCS, on behalf of the United Kingdom health departments, in collaboration with the Dental Schools of the Universities of Birmingham and Newcastle. Maureen O’Brien. London : HMSO, 1994. []
  5. ASDC J Dent Child. 2000 May-Jun;67(3):186-92, 160. A comparison of acidic dietary factors in children with and without dental erosion. O’Sullivan EA, Curzon ME. []
  6. Public Health Nutr. 2004 Feb;7(1A):201-26. Diet, nutrition and the prevention of dental diseases. Moynihan P, Petersen PE. []
  7. Caries Res. 2006;40(3):218-23. Effect of salivary stimulation on erosion of human and bovine enamel subjected or not to subsequent abrasion: an in situ/ex vivo study. Rios D1, Honório HM, Magalhães AC, Delbem AC, Machado MA, Silva SM, Buzalaf MA. []

Diet Reverses Type 2 Diabetes – How Long Have We Known This?

You don’t have to look too hard these days to find WFPB doctors and nutritionists who are reversing people’s type 2 diabetes on a daily basis; nor search too hard to uncover published research papers outlining their successes. However, is this low-tech method of reversing an increasingly common chronic disease, deemed for so long by the medical establishment to be a incurable disease, a new discovery? Not on your nelly1

1935 – Dr I M Rabinowitch

Dr Israel Mordecai Rabinowitch

In a seminal paper published in 1935 2 , Dr Rabinowitch demonstrated that simple dietary changes (increasing the ratio of complex carbohydrates while reducing calorie intake) could reverse type 2 diabetes.

In his summary he states:

I believe that in the data presented here there is incontrovertible evidence that the high carbohydrate-low calorie diet is more effective in controlling diabetes than all other methods of treatment hitherto reported…it is, therefore, more economical from the point of view of the cost of insulin…

Before synthetic insulin was first engineered in 1978 (using E. coli bacteria), insulin was derived from pigs and cattle and was an expensive treatment.

He continues:

“…Experiences with this diet in general support the view that under-nutrition is still an important principle in the treatment of diabetes, except that the term “under-nutrition” has a somewhat different meaning now than in the days before insulin…”

Under-nutrition is seen all around us with the westernised diet of high calorie/low nutrient, processed, largely animal-based foods. Nobody puts it better than Dr Fuhrman 3 when he presents his simple formula:

H = N/C

or

Health Expectancy = Nutrient Intake / Calories

Basically, the more nutrients you consume compared to calories, the healthier you are likely to be and the longer you can expect to live.

Dr Rabinowitch continues:

If, in conclusion, any one of the advantages of this diet may be stressed, it is of the simplicity of treatment...”

We have high-tech solutions for most things now – for the benefit of those industries that want to sell us the latest gadget – phones you can’t open to replace batteries; cars you can’t repair without a bank of expensive computer equipment. Unfortunately, this high-tech tendency spread to food manufacturers who saw that high levels of processing can produce more profits by providing longer shelf-life, cheaper production and distribution methods, and cheaper basic ingredients.*

But the simplest options (low-tech) are best suited to human diets. In nutritional terms, the simplest solution is organic, unprocessed plant foods or, at the least, organic, non-polluted animal foods. The latter are almost impossible to find now, because of the world-wide spread of human pollutants. However, there remain many less natural and human-created problems with eating plants than there are with eating animals.

*See Dr Joel Fuhrman’s brilliant book, Fast Food Genocide: How Processed Food Is Killing Us and What We Can Do about It 4 for a revealing analysis of how food processing came about as a result of the USA’s successes at providing high calorie/long shelf-life/cheap provisions for their military as a result of the two World Wars.

Dr Rabinowitch concludes:

“…and, as I have stated previously 5 the care with which the diabetic will follow treatment will be directly proportional to the simplicity with which it can be carried out.”

If you stick to a WFPB diet, you will get the best results. If you keep ‘treating’ yourself with ‘comfort foods‘, you’ll reduce the effectiveness of the simple dietary solution to your health problems. As with all things, the decision is in your hands.

And before we leave Dr Rabinowitch (1890-1983), I want to point out that this virtually unknown pioneer in the field of nutrition started publishing papers in 1921 and continued publishing a vast array of papers until 1961. A remarkable man.

So, was there no other research data being published between Dr R and the more recent papers of Drs Barnard 6 , McDougall 7 , Fuhrman 8 et al?

Indeed there was.

1958 – Dr Walter Kempner

Dr Kempner published a paper in 1958 9 in which he demonstrated similarly dramatic improvements in and reversals of diabetes, this time via his rice and fruit diet studies.

He published accounts of his work with diabetes, which resulted in the first documented reversals of blindness associated with diabetes (diabetic retinopathy) – indeed, this dramatic improvement occurred in around a quarter of his patients.

Even back in the 1940’s, Dr Kempner was showing that a range of chronic conditions, from kidney disease and hypertension 10  to heart disease and cardiac failure 11 12 could be successfully treated with simple dietary changes, rather than either pharmaceutical or surgical interventions.

Barbara Newborg’s book, Walter Kempner and the Rice Diet: Challenging Conventional Wisdom 13 , presents an interesting account of Dr Kempner’s life and work.

Increasing the amount of dietary fibre is a significant factor in being able to reverse diabetes and other chronic diseases. This was something which the following pioneer discovered during his medical practice and research as a surgeon in Uganda between the 1940’s and 1960’s.

1940’s-1960’s – Dr Denis Burkitt

Known as the Fibre Man, Dr Burkitt was the first to document 14 15 16    the differences in rates of disease (including diabetes) between the populations within rural Africa and in comparison with rates in the United States – with almost negligible cases of these chronic diseases in areas of rural Africa when compared with the widespread (and increasing) cases in the US.

The following WHO chart 17 shows what’s been happening since 1980:

And, as we can see in the following chart 18 , things are predicted to get worse:

Dr Burkitt was prolific in publishing research papers 19 which outlined his explanation of why there were such huge geographical variations in chronic diseases like diabetes – and the primary explanation was (and continues to be) diet. The specific reason to which he pointed was the huge difference between the high fibre content (from unrefined plant foods) in the African diet and the much lower fibre content in the diets of US citizens.

In line with the previous two clinicians mentioned above, he started to publish paper after paper 20 21 22 23 24 that questioned whether these chronic diseases could be prevented by simple dietary intervention, particularly with regard to fibre-content 25 26 27 .  His astute linking of Western dietary patterns with preventable chronic diseases 28 29 30 31    was one of the early inspirations for the likes Dr John McDougall, who did a wonderful videoed interview 32 with Dr Burkitt.

There’s also a free-to-view informative analysis of Dr Burkitt’s life and work, called Denis Burkitt and the origins of the dietary fibre hypothesis 33 , available on-line.

Brian Kellock’s book, Fibre Man: The Life-story of Dr.Denis Burkitt 34 , presents a biography of this highly influential doctor and prolific researcher.

Final thoughts

It’s unlikely that the average person in the street has ever heard of these three pioneers. That’s not such a surprise, really, since there are many inventors, researchers, medical and scientific pioneers who changed our lives without most of us even knowing of their existence.

However, what is more surprising, if not shocking, is that the medical profession appears to have been either utterly unaware or dismissive of their incredible successes with regard to reversing type 2 diabetes and other chronic diseases – something that the very latest and best pharmaceutical/surgical interventions are utterly incapable of achieving. Modern medicine merely treats the symptoms without claiming to be able to cure the disease 35 .

However, things are changing. An increasing number of authorities are now waking up to the fact (and it is a fact) that type 2 diabetes is a chronic disease that can be avoided, treated and reversed by making relatively simple dietary changes.

It’s true that the media 36 37   and the medical profession 38 39 are starting to accept that fasting 40 41  and calorie reduction (regardless, to some extent, of food type) 42 43 can reverse diabetes. However, in order to be able to live a normal life, rather than having to live on will-power and starve oneself while continually counting calories, a WFPB diet is the healthiest and most sustainable means of getting rid of diabetes, as well as reaping the other myriad long-term health benefits that this optimal diet provides 44 .

So, next time you hear of someone saying that diet can treat diabetes, you’ll know that at least three pioneers already knew about this many decades ago. It’s just that hardly anyone was listening to them…



References

  1. Urban Dictionary: Origins of “Not on your nelly”. []
  2. Effects of the High Carbohydrate-Low Calorie Diet Upon Carbohydrate Tolerance in Diabetes Mellitus. Rabinowitch IM. Can Med Assoc J. 1935 Aug;33(2):136-44. PMID: 20319961. []
  3. Health = Nutrient Intake ÷ Calories []
  4. Fast Food Genocide: How Processed Food Is Killing Us and What We Can Do about It by Dr Joel Fuhrman []
  5. OBSERVATIONS ON THE SIGNIFICANCE OF THE CHOLESTEROL CONTENT OF THE BLOOD PLASMA IN DIABETES MELLITUS. Rabinowitch IM. Can Med Assoc J. 1933 Feb;28(2):162-8. No abstract available. PMID: 20319008. []
  6. Dr. Neal Barnard’s Program for Reversing Diabetes: The Scientifically Proven System for Reversing Diabetes without Drugs []
  7. Simple Care for Diabetes by Dr McDougall []
  8. The End of Diabetes by Dr Joel Fuhrman. []
  9. Postgrad Med. 1958 Oct;24(4):359-71. Effect of rice diet on diabetes mellitus associated with vascular disease. KEMPNER W, PESCHEL RL, SCHLAYER C. []
  10. Bull N Y Acad Med. 1946 Jul;22:358-70. Some effects of the rice diet treatment of kidney disease and hypertension. KEMPNER W. []
  11. Treatment of cardiac failure with the rice diet; history of a patient with myocardial aneurysm. KEMPNER W. N C Med J. 1947 Mar;8(3):128-31. []
  12. GP. 1954 Mar;9(3):71-92. Radical dietary treatment of hypertensive and arteriosclerotic vascular disease, heart and kidney disease, and vascular retinopathy. KEMPNER W. []
  13. Walter Kempner and the Rice Diet: Challenging Conventional Wisdom by Barbara Newborg []
  14. East Afr Med J. 1963 Jan;40:1-6. Some geographical variations in disease pattern in East and Central Africa. BURKITT DP, NELSON CL, WILLIAMS EH. PMID: 14017065 []
  15. Cancer Prog. 1963;92:102-13. A CHILDREN’S CANCER WITH GEOGRAPHICAL LIMITATIONS. BURKITT D. PMID: 14282165. []
  16. Sci Basis Med Annu Rev. 1969:82-94. A study of cancer patterns in Africa. Burkitt DP. PMID: 4917845 []
  17. WHO Global report on Diabetes []
  18. Reuters: The global diabetes epidemic in charts []
  19. Lancet. 1969 Dec 6;2(7632):1229-31. Related disease–related cause? Burkitt DP. []
  20. Rev Eur Etud Clin Biol. 1970 Mar;15(3):253-4. Are our commonest killing diseases preventable? Burkitt DP. []
  21. Cent Afr J Med. 1970 Sep;16(9):197-201. A medical research safari: fruits and frustrations. Burkitt DP, Stanfield JP, Church JC. PMID: 5483668. []
  22. Lancet. 1970 Dec 12;2(7685):1237-40. Relationship as a clue to causation. Burkitt DP. PMID: 4098668. []
  23. Br Med J. 1971 May 22;2(5759):450-4. Diverticular disease of the colon: a deficiency disease of Western civilization. Painter NS, Burkitt DP. PMID: 4930390. []
  24. Proc R Soc Med. 1971 Sep;64(9):964-5. Possible relationships between bowel cancer and dietary habits. Burkitt DP. PMID: 5114307.))  ((J Natl Cancer Inst. 1971 Nov;47(5):913-9. Some neglected leads to cancer causation. Burkitt DP. PMID: 5123337. []
  25. Lancet. 1972 Dec 30;2(7792):1408-12. Effect of dietary fibre on stools and the transit-times, and its role in the causation of disease. Burkitt DP, Walker AR, Painter NS. PMID: 4118696. []
  26. Pathol Microbiol (Basel). 1973;39(3):177-86. Diseases of the alimentary tract and western diets. Burkitt DP. PMID: 4198034. []
  27. Trans Med Soc Lond. 1973;89:81-4. Diverticular disease of the colon epidemiological evidence relating it to fibre-depleted diets. Burkitt D. PMID: 4805633. []
  28. Br Med J. 1973 Feb 3;1(5848):274-8. Some diseases characteristic of modern Western civilization. Burkitt DP. PMID: 4568142. []
  29. Clin Radiol. 1973 Jul;24(3):271-80. Some diseases characteristic of modern western civilization. A possible common causative factor. Burkitt DP. PMID: 4592736. []
  30. Proc Nutr Soc. 1973 Dec;32(3):145-9. Epidemiology of large bowel disease: the role of fibre. Burkitt DP. PMID: 4211989. []
  31. JAMA. 1974 Aug 19;229(8):1068-74. Dietary fiber and disease. Burkitt DP, Walker AR, Painter NS. PMID: 4407955. []
  32. Dr. Denis Burkitt interviewed by Dr. John McDougall []
  33. Denis Burkitt and the origins of the dietary fibre hypothesis by CambridgeCore. []
  34. Fibre Man: The Life-story of Dr. Denis Burkitt by Brian Kellock. []
  35. Diabetes Quebec: Diabetes is an incurable disease. []
  36. The Guardian: Radical diet can reverse type 2 diabetes, new study shows []
  37. Medical News Today: Is this the formula for reversing type 2 diabetes? []
  38. BMJ: Losing weight can reverse type 2 diabetes, but is rarely achieved or recorded []
  39. Diabetes.co.uk: Reversing Type 2 Diabetes []
  40. Fasting for Healing – Dr Alan Goldhamer []
  41. The End of Diabetes: The Eat to Live Plan to Prevent and Reverse Diabetes by Dr Joel Fuhrman. []
  42. Lancet. VOLUME 391, ISSUE 10120, P541-551, FEBRUARY 10, 2018: Primary care-led weight management for remission of type 2 diabetes (DiRECT): an open-label, cluster-randomised trial Prof Michael EJ Lean, MD Wilma S Leslie, PhD Alison C Barnes, PGDip Naomi Brosnahan, PGDip George Thom, MSc Louise McCombie, BSc et al. []
  43. NHS: ‘Radical’ low-calorie diet may help reverse type 2 diabetes []
  44. PCRM: Neal Barnard Reversing Diabetes through diet []