Category: Health News

There is ongoing debate about whether the consumption of milk and milk products provides health benefits or alternatively are detrimental to health.

One consideration is important when reviewing publications related to this topic: author/researcher bias.

As an example, I have included an article in this newsletter authored by T. Colin Campbell, PhD.

Some of you may recognize Campbell as the author of “The China Study” which concluded that research conducted in China showed that vegetarian diets were superior to the inclusion of animal protein in the diet.

Independent review of Campbell’s research showed convincingly that the data in the study was selective to prove his hypothesis and in addition Campbell is known to be a big supporter of vegetarian and vegan diets.

Here is an example of some of the rebuttals to Campbell’s study

A1 vs. A2 Protein:

This article also highlights the suggestion that the protein derived from different species of cattle can have different health effects – either good or bad.  This is referred to the difference between A1 and A2 protein:

 

  • A1 beta-casein comes from the most common cow breed that originated in Australia, United States, and Northern Europe. Holstein, Friesian, Ayrshire, and British Shorthorn features A1 beta-casein genetic material. A1 beta-casein can be found on all commercially-prepared milk.
  • A2 beta-casein is protein found in milk produced by ‘old-fashioned’ cows like the Jersey, Charolais, Guernsey, and Limousin. Milk produced by other mammals such as those from human, goat, and sheep is similar to A2 dairy milk mainly due to the presence of proline (6 ,7).

Milk produced by A1 cows supposedly produces opiate-like effects resulting in the development of mild to serious medical conditions (2).

What is BCM7?

BCM7 (Beta-casomorphin-7), an opioid peptide opioid peptide in A1 beta-casein is produced as a result of the breaking off of histidine in the number 67 amino acid chain during digestion(9, 10).

BCM7 is the reason why regular cow’s milk is considered to be a less healthy option than milk containing A2 beta-casein.

The absorption of BCM7 into the bloodstream leads to the high incidence of autism, schizophrenia, and other neurological disorders(11, 12, 13, 14).
 

Also milk contains various hormones which may be detrimental to consume:

https://www.the-scientist.com/uncategorized/whats-in-your-milk-46819

IGF-1 has been associated in some studies with increased height as well as cancer. …

First, cow’s milk contains steroid hormones such as estradiol and testosterone, and peptide hormones such as IGF-1.

Second, drinking milk has been shown to boost serum levels of certain hormones, particularly IGF-1, in humans.

It is also well known that many individuals (approximately 25% of the population in North America) are lactose intolerant and many individuals are reactive to milk.

I have also included an abstract which suggests that milk and milk products are beneficial for human health:

“The totality of available scientific evidence supports that intake of milk and dairy products contribute to meet nutrient recommendations, and may protect against the most prevalent chronic diseases, whereas very few adverse effects have been reported”.

My personal opinion is that cow’s milk is best suited to baby cows, however this is certainly not a black and white consideration.

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There have been some articles circulating in the common press suggesting that skipping breakfast may be detrimental to your health – specifically CVD issues.

These articles are based upon a recently published study: the latest report from the April issue of the Journal of the American College of Cardiology: “Taken together, these studies [showing a positive association between skipping breakfast and CVD and CVD risk factors] as well as our findings underscore the importance of eating breakfast as a simple way to promote cardiovascular health and prevent cardiovascular morbidity and mortality.”

This assertion would of course seem counter-intuitive to those of us who incorporate intermittent fasting into our lifestyle.

For those of you who are practitioners, this topic may come up if some of your patient population has read any of these articles.

Peter Attia MD wrote a great rebuttal to this commentary.  

Peter hosts a great podcast and sends out a weekly newsletter article – here is his website: 

Home – Peter Attia Peter Attia explores strategies and tactics to increase lifespan, healthspan, and well-being, and optimize cognitive, physical, and emotional health. “If you want to know how to live longer, and how to live better, you should be listening to Peter. peterattiamd.com

Here is the content from his newsletter article countering the conclusions of this paper.

(as with many of these types of studies, some key issues included the fact that it was an observational study, bias, confounding factors).

Greetings –

Nota bene: I was pretty pissed off when I wrote this, but don’t let my annoyance detract from the message. Bad science is an abomination. Incompetent news reporting on bad science is worse.

You’ve probably heard that breakfast is the most important meal of the day. “What is less commonly mentioned,” writes Alex Mayyasi in The Atlantic, “is the origin of this ode to breakfast: a 1944 marketing campaign launched by General Foods, the manufacturer of Grape Nuts, to sell more cereal.”

Seventy-five years later, here’s the latest report from the April issue of the Journal of the American College of Cardiology: “Taken together, these studies [showing a positive association between skipping breakfast and CVD and CVD risk factors] as well as our findings underscore the importance of eating breakfast as a simple way to promote cardiovascular health and prevent cardiovascular morbidity and mortality.”

What were the findings? Let’s look at a few newspapers: 

  • “Want to Lower Your Risk for Heart Disease? Eat Breakfast Every Morning” (Healthline)
  • “Eating breakfast? Skipping a morning meal has higher risk of heart-related death, study says” (USA TODAY)
  • “Study: Skipping breakfast increases risk of heart disease mortality by 87 percent (FOX)”

(You may notice that all three headlines imply causality.)

Looks like General Foods was right. Time to reach for the Lucky Charms? Perhaps it’s time to put on our critical thinking cap instead. The actual study, and the media coverage of it, is a part of the Groundhog Day that is observational epidemiology (for more on the limitations of this type of research, check out Studying Studies: Part II). This was a prospective cohort study pulling data from NHANES III, looking at people who reportedly eat breakfast every day to people who never eat breakfast, and then following up with them (about 19 years later on average), tallying up the deaths from CVD and deaths from all causes.

One question to ask about the population studied is: was eating breakfast or not eating breakfast the only difference between these two groups? In other words, were there any confounding factors (for more on confounding, see Studying Studies: Part IV)? The authors reported that, “participants who never consumed breakfast were more likely to be non-Hispanic black, former smokers, heavy drinkers, unmarried, physically inactive, and with less family income, lower total energy intake, and poorer dietary quality, when compared with those who regularly ate breakfast.” Not only that, “participants who never consumed breakfast were more likely to have obesity, and higher total blood cholesterol level than those who consumed breakfast regularly.” They also had a higher reported incidence of diabetes and dyslipidemia. Read that again, please.

While the study used statistical models to “adjust for” many of these potential confounders, it’s extremely difficult (actually, it’s impossible) to accurately and appropriately adjust for what amounts to fundamentally different people. The healthy user bias (or the inverse, an unhealthy user bias) is virtually impossible to tease out of these studies (the healthy user bias is covered in more depth in Studying Studies: Part I). Not only that, you never really know what you’re not looking for. This is typically referred to as residual confounding in the literature, where other factors may be playing a role that go unmeasured by the investigators.

I haven’t even yet mentioned the misleading nature of reporting relative risk — in this case, an associated 87% (reported in the study as a hazard ratio of 1.87) — without reporting absolute risk. The question you should always ask is, 87% greater than what? To get an idea of the associated absolute risk, the number of CVD deaths in the “every day” breakfast group were 415 out of a total of 3,862 people over 16.7 years (that’s an unadjusted rate of 10.7%) while the numbers for the “never” breakfast folks were 41 CVD deaths out of a total of 336 people over 16.7 years (unadjusted rate of 12.2%). That’s an absolute difference of 1.5% over almost 17 years (annually, this is an absolute difference of 0.09%). Granted, this is before adjustment of the myriad confounders (including the biggest “risk factor” for CVD death, age, in which the “never” breakfast group was younger on average at baseline), but it gives you an idea that we’re looking at small differences even over the course of a couple of decades. This looks a lot difference on paper than an associated 87% increased risk of CVD death. (For more on absolute risk and relative risk, see Studying Studies: Part I.)

There’s more: 

  • What were the participants actually eating for breakfast? We don’t know. The investigators didn’t have information about what foods and beverages they consumed.
  • Did participants change their breakfast eating (or abstaining) habits over the course of almost 20 years? We don’t know. Information on breakfast eating was only collected at baseline.
  • Could there be errors in the classification of the causes of death in the participants? It’s possible.
  • What constitutes skipping breakfast? Was it the timing of the first meal of the day? We don’t know. Participants were asked, “How often do you eat breakfast?” but there was no definition of what that means, exactly.

What’s more likely: reported skipping breakfast was a marker for a lifestyle and environment that may have predisposed these people to a higher risk of CVD death or that skipping breakfast itself causes CVD death?

Go ahead and skip all the breakfasts you want. And please forward this to the next 10 people who tell you it’s unhealthy to do so.

– (Pissed off) Peter

For a list of all previous weekly emails, click here.

podcast | website | ama

It has been suggested in the literature that consumption in the diet of methionine – an amino acid such as in animal protein may have a negative effect on healthspan and potentially lifespan.

It has also been suggested that dietary restriction (DR) of methionine is a good lifestyle choice for healthy aging.

This presents a problem for those of us that are omnivores and include quality animal protein in our diets.

A suggested solution to this quandary is to consume supplemental glycine, a readily available and inexpensive amino acid.

Following are representative abstracts on these topics.

It is worth noting that with respect to cancer that glycine may stimulate growth so dietary glycine restriction may be of benefit.

Prog Mol Biol Transl Sci. 2014;121:351-76. doi: 10.1016/B978-0-12-800101-1.00011-9.

The impact of dietary methionine restriction on biomarkers of metabolic health.

Orgeron ML1, Stone KP1, Wanders D1, Cortez CC1, Van NT1, Gettys TW1.  

Abstract

Calorie restriction without malnutrition, commonly referred to as dietary restriction (DR), results in a well-documented extension of life span. DR also produces significant, long-lasting improvements in biomarkers of metabolic health that begin to accrue soon after its introduction. The improvements are attributable in part to the effects of DR on energy balance, which limit fat accumulation through reduction in energy intake.

Accumulation of excess body fat occurs when energy intake chronically exceeds the energy costs for growth and maintenance of existing tissue. The resulting obesity promotes the development of insulin resistance, disordered lipid metabolism, and increased expression of inflammatory markers in peripheral tissues. The link between the life-extending effects of DR and adiposity is the subject of an ongoing debate, but it is clear that decreased fat accumulation improves insulin sensitivity and produces beneficial effects on overall metabolic health. Over the last 20 years, dietary methionine restriction (MR) has emerged as a promising DR mimetic because it produces a comparable extension in life span, but surprisingly, does not require food restriction.

Dietary MR also reduces adiposity but does so through a paradoxical increase in both energy intake and expenditure. The increase in energy expenditure fully compensates for increased energy intake and effectively limits fat deposition. Perhaps more importantly, the diet increases metabolic flexibility and overall insulin sensitivity and improves lipid metabolism while decreasing systemic inflammation. In this chapter, we describe recent advances in our understanding of the mechanisms and effects of dietary MR and discuss the remaining obstacles to implementing MR as a treatment for metabolic disease.

KEYWORDS:

Amino acid sensing; Animal models; Dietary protein; Insulin sensitivity; Obesity

Biochemistry/Molecular Biology

Dietary glycine supplementation mimics lifespan extension by dietary methionine restriction in Fisher 344 rats

Joel Brind,Virginia Malloy,Ines Augie,Nicholas Caliendo,Joseph H Vogelman,Jay A. Zimmerman, and Norman Orentreich
Abstract

Dietary methionine (Met) restriction (MR) extends lifespan in rodents by 30–40% and inhibits growth. Since glycine is the vehicle for hepatic clearance of excess Met via glycine N-methyltransferase (GNMT), we hypothesized that dietary glycine supplementation (GS) might produce biochemical and endocrine changes similar to MR and also extend lifespan. Seven-week-old male Fisher 344 rats were fed diets containing 0.43% Met/2.3% glycine (control fed; CF) or 0.43% Met/4%, 8% or 12% glycine until natural death.

In 8% or 12% GS rats, median lifespan increased from 88 weeks (w) to 113 w, and maximum lifespan increased from 91 w to 119 w v CF. Body growth reduction was less dramatic, and not even significant in the 8% GS group. Dose-dependent reductions in several serum markers were also observed. Long-term (50 w) 12% GS resulted in reductions in mean (±SD) fasting glucose (158 ± 13 v 179 ± 46 mg/dL), insulin (0.7 ± 0.4 v 0.8 ± 0.3 ng/mL), IGF-1 (1082 ± 128 v 1407 ± 142 ng/mL) and triglyceride (113 ± 31 v 221 ± 56 mg/dL) levels compared to CF.

Adiponectin, which increases with MR, did not change in GS after 12 w on diet. We propose that more efficient Met clearance via GNMT with GS could be reducing chronic Met toxicity due to rogue methylations from chronic excess methylation capacity or oxidative stress from generation of toxic by-products such as formaldehyde. This project received no outside funding.

Royal jelly from the bee hive has been suggested to provide a range of health benefits to humans: I personally have found it to be of benefit for sleep as well as adrenal support.

Here are some of the suggested health benefits of royal jelly from the website Self Hacked:

Although chemically diverse, royal jelly mostly acts by [R, R]:

  • Fighting microbes and reducing inflammation, mostly via royalisin (10H2DA)
  • Fighting bacteria through jelleines
  • Boosting antioxidant defense, via flavonoids [R]
  • Royal Jelly Boosts Reproductive Health
  • Royal Jelly May Help with Diabetes3) Royal Jelly Reduces Chemotherapy Side Effects
  • Royal Jelly May Improve Mental Health
  • Royal Jelly May Increase Red Blood Cells
  • Royal Jelly Reduces Cholesterol
  • Royal Jelly Reduces Allergies and Th1 Dominance
  • Royal Jelly Assists Wound Healing9) Royal Jelly Boosts Immunity and Fights Infections
  • Royal Jelly Protects the Brain
  • Royal Jelly Boosts Collagen for Skin and Hair Health
  • Royal Jelly May Boost Longevity
  • Royal Jelly Protects Joints
  • Royal Jelly May Protect the Liver
  • Royal Jelly May Fight Tumors

In the following article and related abstract, it is suggested that royal jelly can impact on stem cell vitality:

Researchers at Stanford University found that the main active component in royal jelly, a protein called royalactin, activates a network of genes that bolsters the ability of stem cells to renew themselves. It means that, with royalactin, an organism can produce more stem cells to build and repair itself with.

Here is the article and abstract

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In recent newsletter articles I have discussed the significant growing health issue of NAFLD – Non-Alcoholic Fatty Liver Disease which is now present in approximately 25% of the general population.

From the website: GMWatch.org:

“Risk factors for NAFLD include being overweight or obese, having diabetes, or having high cholesterol or high triglycerides (a constituent of body fat) in the blood. However, some people develop NAFLD even if they do not have any of these known risk factors.

Symptoms of NAFLD include fatigue, weakness, weight loss, loss of appetite, nausea, abdominal pain, spider-like blood vessels, yellowing of the skin and eyes (jaundice), itching, fluid build-up and swelling of the legs and abdomen, and mental confusion”.

Excessive consumption of sugar – especially fructose can also contribute to the development of NAFLD.

Another potential cause of the dramatic increase in the incidence of NAFLD in the general population is exposure to glyphosate, present in the herbicide Roundup:

From the same article mentioned above from GMWatch.org:

Roundup causes non-alcoholic fatty liver disease at very low doses

“The weedkiller Roundup causes non-alcoholic fatty liver disease at very low doses permitted by regulators worldwide, a new peer-reviewed study shows. The study is the first ever to show a causative link between consumption of Roundup at a real-world environmentally relevant dose and a serious disease”.

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Trying to understand why we need to sleep has been a topic that researchers have been pursuing for many decades: why do we spend approximately 1/3 of our lives sleeping?

There has been some very interesting research published in the last several years which helps to give us some insight into this intriguing question.

I recently listened to a podcast on the topic of sleep in which Peter Attia, MD was interviewing Matthew Walker, PhD professor of neuroscience at UC Berkeley and an expert on sleep.

Info on Peter and his podcast are included at the end of this article.

This was a lengthy interview: some three hours so it has been broken down into three podcasts.

I came away from listening to these podcasts completely reshaping my understanding of the health impact of adequate sleep: the rapidity of cognitive and performance deterioration after even one night of poor sleep is shocking.

One of the topics that I found most interesting was the link between sleep deprivation and the potential development of Alzheimer’s.

A recent discovery is the existence in the brain of the “Glymphatic System”.

Glymphatic of course sounds similar to Lymphatic – and that is a good comparison in that the Glympatic system functions in the brain like the Lymphatic system functions in the body.

How this impacts on Alzheimer’s is as follows:

Amyloid proteins are present in everyone’s brain, and what happens during sleep is these amyloid proteins are transported out of the brain by the Glympatic system.  If sleep duration is compromised, the clearing effect is diminished which can lead to an accumulation of amyloid proteins.

And of course Alzheimer’s is a complex disease process so like many other factors, lack of sleep may be a contributing factor to the development of Alzheimer’s.

We have all heard of individuals who boast of being able to get by on restricted sleep: five hours or whatever.

Matt in one of the podcasts made reference to two high profile politicians from the past that boasted about this, and lived their lives in this manner (restricted hours of sleep).

These two individuals were Ronald Regan and Margaret Thatcher, both of whom ended up developing dementia/Alzheimer’s in the latter stages of their lives.

In conjunction with these podcasts, I also came across an article published in the Natural Medicine Journal:

Sleep Deprivation and Alzheimer’s Disease:

I don’t know about you, but I think I am going to bed early tonight…

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