Category: Anti-aging

Enzogenol, the signature ingredient in our recently launched GenZogenol-R Healthy Aging formulation has been shown in rodent studies to lengthen telomeres by over 40% and to extend healthspan significantly as well as extend lifespan by 18% – this would equate to 15 years in humans.

We cannot assume of course that results in rodents will be duplicated in humans, however my personal philosophy has always been that when I come across an ingredient or formulation that directly targets the health of DNA and has such a significant impact on healthspan – and potentially lifespan – I am taking it!

We are working towards human clinical trials to corroborate these results, and that is a key concept with our company: we utilize third party technologies and lab tests (such as telomere length and health as well as age related methylation degradation) to corroborate the efficacy of our formulations.

GenZogenol-R targets the aging process at a DNA level

Two key animal studies:

  • In a rat study, Enzogenol LENGTHENED telomeres by more than 40%
  • In a mouse study in middle aged mice, one cohort was supplemented with Enzogenol and the other cohort was not
  • The cohort group supplemented with Enzogenol achieved an extension of healthspan as well as lifespan (18% lifespan extension which in humans would equate to 15 years)


Key GenZogenol-R Applications:

Read More:

https://www.dropbox.com/s/6hyxd3uk9ip09qs/GenZogenol-R%20Article.docx?dl=0

I am concerned about the increasing popularity of the vegan movement and vegan diets with respect to its potential impact on individuals’ health.

My personal opinion and my experience working with patients is that initially individuals who adopt a (healthy) vegan diet may realize some health benefits, however over the long term there is a significant potential that these individuals may develop nutrient deficiencies which may have profound effects on health.

From my perspective, there are a couple of considerations to this:

Firstly, every individual is biochemically and metabolically unique and a vegan diet may not be appropriate for a specific individual.  This is the same consideration with respect to any diet, whether it be low carb/high fat, vegetarian – or whatever.

The second consideration is the fact that most individuals simply do not have the knowledge and expertise to understand how to assess whether they are developing deficiencies, or how to supplement to address these deficiencies or prevent them.

I recently presented a three hour Master Class lecture to 4th year Naturopathic students at our local Naturopathic school: Boucher.

The topic of the lecture presentation covered ketosis, the ketogenic diet, intermittent fasting, time restricted feeding – but also information on the Fasting Mimicking Diet developed by Valter Longo, PhD.

If you are not familiar with the Fasting Mimicking Diet (FMD), the concept is that for a limited number of days during any month if you consume a restricted number of calories of specific types of food, it has the effect of providing a CRM (Caloric Restriction Mimetic) influence on the metabolism for the whole month.

And Longo and his colleagues have published a considerable number of studies to back up his hypothesis.

The one negative about the program is that they recommend accessing (expensive) prepared meals from a provider for the fasting days in a set up similar to Weight Watchers.

Also in the lecture presentation, I talked about some of the issues related to vegan diets (deficiencies) – and also with animal protein consumption (the primary concern being an increase in IGF-1 insulin like growth factor levels which can stimulate cell growth and division – and some ways to counteract this mechanism which I will detail in a separate article).

Today I wanted to share an article from the Daily Mail newspaper in the UK detailing Virpi Mikkonen who is a high profile poster girl for the meat-free revolution and a social media guru and how she confessed that a vegan diet ruined her health and brought on early menopause.

Also I am including some information from my Boucher lecture regarding some of the potential nutrient deficiencies associated with a vegan diet.

Individuals choose specific diets for different reasons: for ethical and environmental issues (common with the vegan community), they buy into a fad diet which has become popular – or hopefully like myself and I would presume many practitioners reading this article that have biohacked their metabolism to determine the best diet to optimize their health and quality of life.

For myself, a LCHF (low carb / high fat) / ketogenic diet works optimally: I do not stay in ketosis continuously but I have adapted my metabolism so that it can switch back and forth effortlessly between burning fat and sugars.

I am of the opinion that this metabolic flexibility is something that all individuals can benefit from, provided their metabolism and health will allow them to stay in a continuous state of ketosis to initially make this transition to being keto adapted, which takes about six weeks.

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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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