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Dean Pomerleau

Cold Exposure & Other Mild Stressors for Increased Health & Longevity

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Matt from Vice summarizes pretty well the origins of the exceptional wim hof's resistance to extreme cold:

 

  1. Abundance of BAT
  2. Control of Adrenaline
  3. Mental concentration
  4. Pranayama

1 and 2 are complementary, we know from metabolism that mTOR in BAT is activated by the thermal stimulus to synthetize more BAT cells. Also, Noradrenaline=Norepinephrine (NE) is released by cold temperature itself. A conscious control on Adrenalin and NE (apparently exhibited by Wim hof during his voluntary lab poisoning) would but amplifiy mTOr activity in BAT.

3 is partly physiologically plausible, since we know from Rhonda Patrick that it is possible to express a gene by simply concentrating on it ( I don't have the scientific references but  Rhonda supports all of her affirmations).

4 is more into the metaphysical metabolism, the subtle energy which presumably governs all bodily activities and metabolic reaction, the so called 'Prana', I'm aware of no mechanistic explanation about this.

 

Mental power backs it all up. There is no fear of cold, on the contrary there is the opposite, worshipping of cold. This mental attitude allows, even by simple frequent and extreme exposure, an unflinching amplification of all the metabolic effects related to thermal stimulus.

 

Also, a very strong point in Wim's reasonings (even though qualitative) is that he showed that his feats are (at least in part) repeatable by other people. Guys in his group get exposed regularly to extreme cold.

Edited by mccoy

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After reading most of the posts, I want to bring another perspective for glucose and weight control. When people ask me why I am so thin despite I eat in abundance, I often reply with "my brain burns all the excess calories because I'm smart" with some evil laugh. Well, rather than being smart, being mentally active all the time could work for me especially considering this anecdote of mine:

I had a period of time in the past (10 months) where I did't exercise at all and very sedentary, ate a standard western diet ad lib low on fruits and vegetables high in fat and protein but not so junky. However, I was able to maintain a BMI of 20, and the reason was probably due to me being mentally very active with the stock exchange during day and night. 

 

I'm not an expert on brain but I know that it's mostly fat which burns lots of glucose and lots of it. Here goes my speculation of why humans and probably other intelligent mammals have less BAT than lesser end mammals. It's because evolutionary we sacrificed most of our BATs in order to create excess calories for brain to burn and developed better housing, invented clothing etc. for preventing cold exposure. Not a bad thing considering actually brain can be a great source as a glucose sink as you guys have described.

 

Maybe thought exposure (TE) is also a very effective way of increasing metabolic rate and controlling glucose metabolism apart from CE. It might be a valid option if you don't want the hassle of CE or even better you can combine both of them and play chess in a cold environment - thought exposure while cold exposure (TEwCE).

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Burak, I've actually had some similar thoughts.  My full time job involves non-stop critical thinking and problem solving pretty much all day every day, and when I'm not doing that I am often focused on other research and personal projects.  Often I am so focused that I just don't want to break to consume food.  Interestingly enough, I too was once a full time trader, and was completely absorbed in the markets to the point where I would even dream about various things that were likely coming (which is one theme in the market wizards books).

 

The brain does burn quite a few calories, but it seems that "thinking hard brain" doesn't burn many more calories than "at rest brain" (maybe because the brain is never really at rest?).  Then again, there is a certain level of uncertainty about this.

 

See:  

Does Thinking Really Hard Burn More Calories?

 

Unlike physical exercise, mental workouts probably do not demand significantly more energy than usual. Believing we have drained our brains, however, may be enough to induce weariness.

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Gordo, I'm not convinced about we cannot burn more while demanding mental workouts as there is not conclusive evidence. It might be personal, but in my university years I often got some hypoglycemic symptoms like feeling lack of energy (and even lack of appetite which can be a sign of increased ketone levels as a result of depleted glycogen stores since I didn't have too much muscle to store it in large quantities), trembling and feeling cold etc. after 3-4 hours of exams which I can assure you is probably the most mentally demanding workouts given specific time.

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I have realized that Medium Chain Triglycerides are not specifically included in Dean's BAT activator list. My reasoning they might be working is that baby mammals have the greatest BAT activity and milk provides some MCT, maybe to further increase heat production in order to protect them from cold during their early ages. This is probably another reason why atherosclerosis rate increases as we age due to lack of BATs, and as a result saturated fatty acids and triglycerides tend to stay long in the blood stream as mentioned before.

 

MCTs are also very popular nowadays for their ability of increasing calorie burning. By BAT rule, indeed, I obtained these two articles that support this:

 

https://www.ncbi.nlm.nih.gov/pubmed/25716560

https://www.ncbi.nlm.nih.gov/pubmed/22790949

https://www.ncbi.nlm.nih.gov/pubmed/3613876

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Dean Pomerleau: 

Here is another BAT Rule1 example, this time involving the dietary flavonoid Luteolin (LU), which is high in the following foods (ranked highest to lowest per 100g) based on this list:

 

 

Artichoke extract appears to be another good source of luteolin.

--------------------

https://examine.com/supplements/artichoke-extract/

 

 

Artichoke extract contains:

  • Luteolin (27.71-215.52mg/kg) and the glycoside Luteolin-7-O-Glucopyranoside, the latter being known as Cynaroside.[6] These two are seen as the active Luteolin compounds, and are named after Cynara due to this

  • Other Luteolin compounds such as Luteolin 7-O-rutinoside, Luteolin 7-O-glucoside, and Luteolin 7-O-glucuronide;[4] all Luteolin compounds collectively range from 24.6-73.8g/kg, or 2.5-7.4% (variance depending on cultivar) and most being 7-O-glucoside[4]

  • Caffeoylquinic acids including Cynarin (aka. 1,3-dicaffeoylquinic acid)[6] and others such as 1-O-caffeoylquinic acid, 3-O-caffeoylquinic acid, 4-O-caffeoylquinic acid, 5-O-caffeoylquinic acid, and Caffeic acid.[4] Total caffeoylquinic acids range from 3139.02-7270.11mg/kg (0.3-0.7%)[4]

  • Chlorogenic Acid (aka. 5-O-caffeoylquinic acid)[7][6] ranging from 106.39-423.94mg/kg (0.01-0.04%)[4]

  • Apigenin (as 7-O-glucuronide, 7-O-glucoside, and 7-O-rutinoside)[4] with total Apigenin compounds ranging from 43.74-6477.68mg/kg (0.004-0.650%)[4]

  • Sterols including Beta-Sitosterol, Stigmaterol, and Campesterol[8]

 

-----------------------

http://etd.fcla.edu/UF/UFE0020087/sarawek_s.pdf

 

The results from Table 2-5 showed that the caffeoylquinic acids were the predominant phenolic compounds of the artichoke extract, with 5-O-caffeoylquinic acid showing the highest amount. The predominant flavonoid was luteolin-7-O-glucoside, followed by luteolin-7-Oglucuronide.

---------------------------

 

Table 2-5. Amounts of caffeoylquinic acids and luteolin derivatives expressed as milligram per gram of dried extract.

Compound Amount of compounds in artichoke extract (mg/g) mean ± SEM

 

5-O-caffeoylquinic acid (chlorogenic acid) 8.71 ± 0.59

1,3-di-O-caffeoylquinic acid (cynarin) 2.47 ± 0.54

luteolin-7-O-glucoside 3.60 ± 0.62

luteolin-7-O-glucuronide 2.08 ± 0.73

 

----------------------------

See also:

"Euromed Artichoke Extracts"

http://www.euromed.es/pdfs/artichoke.pdf

 

"Luteolin-rich artichoke extract protects low density lipoprotein from oxidation In vitro"

https://www.researchgate.net/publication/13483079_Luteolin-rich_artichoke_extract_protects_low_density_lipoprotein_from_oxidation_In_vitro

 

"Flavonoids from Artichoke (Cynara scolymus L.) Up-Regulate Endothelial-Type Nitric-Oxide Synthase Gene Expression in Human Endothelial Cells" http://jpet.aspetjournals.org/content/310/3/926.full

Edited by Sibiriak

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I have realized that Medium Chain Triglycerides are not specifically included in Dean's BAT activator list. My reasoning they might be working is that baby mammals have the greatest BAT activity and milk provides some MCT, maybe to further increase heat production in order to protect them from cold during their early ages. This is probably another reason why atherosclerosis rate increases as we age due to lack of BATs, and as a result saturated fatty acids and triglycerides tend to stay long in the blood stream as mentioned before.

 

MCTs are also very popular nowadays for their ability of increasing calorie burning. By BAT rule, indeed, I obtained these two articles that support this:

 

https://www.ncbi.nlm.nih.gov/pubmed/25716560

https://www.ncbi.nlm.nih.gov/pubmed/22790949

https://www.ncbi.nlm.nih.gov/pubmed/3613876

 

Nice.  Another +1 for EVOO, and possibly a +1 for coconut oil which most in the plant based whole food world consider junk food, but many others laud for its health benefits.

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Humans have three times more brown body fat

A study of 3,000 PET-scans yields new data on the proportion of brown fat

https://www.sciencedaily.com/releases/2017/03/170301105500.htm

 

"Compared to white fat, brown body fat burns through energy at an extraordinary rate. However, until now the proportion of brown fat in humans was thought to be quite small. Now a study has shown that the quantity of brown fat in humans is three times greater than previously known. As a consequence, new obesity and diabetes drugs that activate brown adipose tissue are expected to be more effective."

 

 

Active brown fat during 1FDG-PET/CT imaging defines a patient group with characteristic traits and an increased probability of brown fat redetection

  1. Carlos Gerngroß 
  2. Johanna Schretter 
  3. Martin Klingenspor 
  4. Markus Schwaiger 
  5. Tobias Fromme

 

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New study with a twist on catechins:

Tea catechin and caffeine activate brown adipose tissue and increase cold-induced thermogenic capacity in humans

These guys took things to a new level by adding cold exposure to the mix:

 

Before and after ingestion of the catechin beverage 2 times/d for 5 wk, cold-induced thermogenesis (CIT) after 2 h of cold exposure at 19°C [66F], which is proportional to BAT activity, was examined

 

Conclusion: Orally ingested tea catechin with caffeine acutely increases EE associated with increased BAT activity and chronically elevates nonshivering [cold induced thermogenesis] (CIT), probably because of the recruitment of BAT, in humans.

 

I don't know why I stopped drinking green tea for a while, but I am going to start back up again.  I've also read that white tea is actually highest in catechins, need to do more research to find the type with the highest levels...

 

-Gordo

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New reason not to consume alcohol:

Chronic alcohol consumption decreases brown adipose tissue mass and disrupts thermoregulation: a possible role for altered retinoid signaling

" Our work highlights a hitherto uncharacterized effect of alcohol on BAT function, with possible implications for thermoregulation and energy metabolism in drinkers."

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Green tea was already on the list, but it is good to see that the evidence is accumulating. As for the alcohol, there is no doubt that the chronic alcohol consumption is bad. The real question is, what is the short and long term effects of 1-2 drinks on a regular basis and especially for red wine?

 

I also want to ask a question about activating BAT:

What is the gold standard here? I mean, what do we need to show that a dietary component activates BAT? Because everytime I eat popcorn, in just 10-15 minutes my body turns to a furnace. It is probably because of its high GI content I assume, but can we consider it as a BAT activator, well at least for me? I think the difference can be the net effect, i.e. I just burn glucose from popcorn and there is nothing gained, but with tea I burn what was already in the bloodstream so there is some net gain.

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Gordo, I wonder whether the BAT activation effect occurs with the cacao epicatechins as well. Cacao also contains catechins, or (+) catechin, but in smaller amounts.

 

I hit upon this article first, on commercial teas:

 

Catechin Content of 18 Teas and a Green Tea Extract Supplement Correlates With the Antioxidant Capacity

 

Table 2 and 3 must be interpreted, but mg/100 ml, like explained in the text, is the content of a 100 ml cup where a bag of tea has been brewed.

 

There are really not very large differences in black and green teas, although differences in specific brands may be huge. And usually green has more catechins than black.

 

Now, the interpretation and comparative discussion with cacao should be done in what terms? Catechin and epipcatechin monomers? polymers? Total catechins? total polyphenols?

More than one of the above and which ones?

 

My gut feeling (sometimes this is more scientific than current literature)  is that both are good in total polyphenols, but the amounts in the specific groups govern slightly different health benefits.

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Interesting talk and some new research on Ketones and BAT.

 

Dr. Benjamin Bikman - 'Insulin vs. Ketones - The Battle for Brown Fat'

 

 

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KenB, thanks for posting the Bikman video link. The video started a bit slow / basic - though well presented, but the climax was worth the wait. It looks like the list of BAT activators in this thread should include carbohydrate restriction/keto diet. Protein restriction is already listed with leucine singled out as critical. If one consider that leucine is highly insulinogenic then Bikman's claim that recent research shows insulin suppresses BAT activity adds additional support for the idea of restricting protein/leucine. But reducing high glycemic carbs ought to be a prime target as they are even more insulinogenic.

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While doing some search on PubMed to find if there is any side effect of excessive black pepper consumption (since I like and consume it a lot), I stumbled upon this study:

 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5259784/

 

Just wow! I didn't understand some of the technical details, but even just looking at the graphs blew my mind. Is this stuff really that powerful? I was planning to reduce my black pepper consumption speculating that it might damage my liver and metabolism in the long run, but it seems like there are no adverse effects.

 

I want ask if anyone of you know how much black pepper we need to consume to get -10 or 30- μM piperine?

 

They also mention piperine as a curcumin extract or a curcumin derivative, and they also have this passage:

---

We previously reported that curcumin stimulated glucose uptake in skeletal muscles. The clinical usefulness of curcumin has been limited due to its low bioavailability caused by poor absorption and faster metabolic alteration. It was reported that piperine enhanced curcumin’s effect not only by reducing curcumin’s metabolic breakdown, but also by increasing the absorption of curcumin in intestine. Piperine is a structural analogue of curcumin, and its molecular weight is smaller than curcumin. In the point of human application, small molecule is more useful. Therefore, piperine is a promising molecule for the development of diabetes by enhancing curcumin’s beneficial metabolic effect.

---

 

Am I missing something? Why do they refer piperine as a curcumin extract or derivative?

 

 

 

Edit: Piperine content of black pepper can be as high as 9% (http://onlinelibrary.wiley.com/doi/10.1111/1541-4337.12246/full). However, I could not find a source to see how much dietary black pepper we should eat to reach these effective levels. I will continue to eat them ad-lib.

Edited by Burak

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Burak, the molecular structures of piperine and curcumin appear to be different, so I too am perplexed by the contention that piperine is a curcumin derivative.

 

It's very interesting to remark that basically piperine activates AMPK, which is an inhibitor of the mTOR metabolic master switch.

 

We all know that switching mTOR down in the organs constitutes a powerful longevity-enhancing condition. After all, that's what rapamycin does.

 

Do we have an harmless alternative of rapamycin here? Searching mTOR in the above article gave no results.

 

A search of piperine + mTOr in google gives a few results but since we lapse into OT here, I'm going to open another thread.

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This is a pretty old study, but I found it interesting particularly in light of the recent forum discussions about salt/sodium intake:

 

Influence of sodium intake on thermogenesis and brown adipose tissue in the rat.

These data show that increasing sodium intake... has very little effect on food intake or resting metabolic rate, but causes a marked increase in thermogenic capacity and responses to food or noradrenaline, probably because of an increase in active BAT mass. Changes in plasma ion concentrations or osmolarity, therefore, could be involved in the thermogenic response to food.

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If anyone's interested:

 

Thesis by Maarten Vosselman - ‎2014  pdf

Strategies to activate brown adipose tissue in humans

 

Table of Contents

Chapter 1 General Introduction       7
Chapter 2 Energy dissipation in brown adipose tissue: from mice to men      19
Chapter 3 Brown adipose tissue activity after a high caloric meal in humans  37
Chapter 4 Systemicβ-­‐adrenergic stimulation of thermogenesis is not accompanied by brown adipose tissue activity in humans 53
Chapter 5 Reduced brown adipose tissue activity in endurance trained compared to lean sedentary men  73
Chapter 6 Frequent extreme cold exposure and brown fat and cold-­‐induced thermogenesis :a study in a monozygotic twin    

  ["The Iceman"]   93
Chapter 7 General Discussion 111
Summary     127
Valorisation  135
Dankwoord  141
Curriculum Vitae 147
List of publications  151

Edited by Sibiriak

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From the above thesis:

 

REDUCED BROWN ADIPOSE TISSUE IN  ENDURANCE ATHLETES
 

Abstract 

It has now been  unequivocally demonstrated that humans possess functional brown adipose tissue (BAT) and that human BAT can be recruited upon chronic cold stimulation. Recruitment of BAT has been postulated as a potential strategy to  counteract  the  current global obesity epidemic. Recently, it was shown in rodents that endurance exercise training could stimulate the recruitment  of brown-­‐like adipocytes within WAT via the myokine irisin, which is the cleaved circulating product of the type 1 membrane protein FNDC5. We here tested cold-­‐stimulated BAT activity via [18F]FDG-­‐PET-­‐CT-­‐imaging and browning of subcutaneous WAT by means of gene expression in  twelve endurance trained athletes and twelve lean sedentary males. Indeed, mRNA expression of  NDC5 in skeletal muscle was significantly higher in endurance athletes.However, cold-­‐induced  BAT activity was significantly lower  in athletes and no differences in gene expression of classical brown and beige adipocyte markers were detected between the groups. These results thus indicate that chronic endurance exercise does not lead to brown and beige adipocyte recruitment, and rather is associated with lower metabolic activity of BAT in humans.   

 

[p.74]  [emphasis added]  [see text for  possible explanations for this finding.]

Edited by Sibiriak

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Sibiriak, I was going to post that study in this topic, but for some reason I forgot. It is very interesting.

 

https://www.ncbi.nlm.nih.gov/pubmed/26189600

https://www.ncbi.nlm.nih.gov/pubmed/25500952

 

Maybe endurance athletes were feeling warm due to all these exercises or the body tries to keep BAT volume as low as possible in order to prevent energy wasting. For me, eating excessive is the primary factor for BAT activation regardless I do CE or eating healthy or not. This provides greater glucose control but can be annoying if you try to gain some weight.

Last summer, I was planning to put on some weight while the weather was hot, but ended up losing more probably due to I was not eating enough fat. This time, I will try this with more olive oil without resorting to high GI foods. I am pretty much convinced that having low body fat especially if you are underweight can cause dietary toxicities such as overreaction to chili peppers, headaches from some herbal teas and more importantly hormonal problems from dairy products.

I believe this is one of the reasons why CR fail to produce conclusive results on humans(longer life) since we live in a highly polluted planet and if you do not have some fats to absorb these toxins and pollutants and give body more time to detox itself, then you are in big trouble.

Edited by Burak

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Burak: Maybe endurance athletes were feeling warm due to all these exercises or the body tries to keep BAT volume as low as possible in order to prevent energy wasting.

 

 

In the thesis linked above, Vosselman discusses  possible explanations for the lower BAT activity of endurance athletes.   He found that the endurance athletes had greater vasoconstriction than the lean sedentary folks which functioned as a kind of insulation.   He refers to other studies wherein the authors hypothesized that  endurance conditioning may  promote  vascularization of  muscle  tissue and/or alter tissue sensitivity to circulating catecholamines thereby increasing the capacity for vasoconstriction.

 

Also:

Despite increased insulation, there  was a trend for lower core temperature during the cold exposure in the athletes, suggesting that athletes might tolerate lower internal body temperatures, which has been demonstrated previously in long distance runners.
Edited by Sibiriak

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I am pretty much convinced that having low body fat especially if you are underweight can cause dietary toxicities such as overreaction to chili peppers, headaches from some herbal teas and more importantly hormonal problems from dairy products.

I am scratching my head on this one. Why would you think that having low body fat would lead to dietary toxicities, let alone the various things you list (which are not dietary toxiciteies, NB)?

 

I believe this is one of the reasons why CR fail to produce conclusive results on humans(longer life) since we live in a highly polluted planet and if you do not have some fats to absorb these toxins and pollutants and give body more time to detox itself, then you are in big trouble.

Of course, the CR nematodes, flies, mice, rats, rabbits, etc also live on this planet ...

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Micheal, you are right that I used the expression "dietary toxicities" in a wrong way, but I think you got what I mean. 

 

First one should be obvious right? There is a difference between 90kg vs. 55kg man affecting from alcohol or medicine or in my case exogenous hormones. I also remember that there are lots of fat soluble toxins such as PCBs etc., and if you are obese it is logical to think that you get less damage when you eat i.e. fish since some of them will be absorbed by fat cells and you will have less of it in your bloodstream after ingestion.

 

Second one is a speculation at the moment, based on above logic. Humans life span is long, meaning more time to expose to toxins, pollutants etc., and add that to CR people have smaller liver and less detoxifying capacity (right?). I think it is worth investigating as a negative aspect of having a CR body, because maybe having a little bit of more fat (also muscle and liver mass) by doing a little bit of less CR can be more optimal.

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Burak:   I was going to post that study in this topic, but for some reason I forgot. It is very interesting.

 

https://www.ncbi.nlm...pubmed/26189600

 

 

I've started the daunting task of reading through this topic from the beginning --it's truly a gold mine--and I noticed that Dean P. had posted about that study way back.

 

Dean Pomerleau:  As discussed in this post, this study (PMID 24506871) found that endurance exercise results in the 'browning' of white adipose tissue, but via a different pathway than cold exposure (Irisin vs. FGF21). Here is the graphical abstract from PMID 24506871 showing the two different pathways:

 

But in contrast, this study [1], found that endurance trained young male athletes had lower BAT activity in response to cold exposure than lean, sedentary young men. It also found that while the precursor to Irisin (FNDC5) was elevated in athletes, Irisin itself was no different between the athletes and the couch potatoes, in apparent contradiction to the study above which found exercise increased Irisin which in turn converted WAT to BAT. So it appears the jury is still out on whether exercise really does increase BAT.

 

#86  Posted 29 February 2016 - 03:35 AM

 

I try to search to see if something has already been posted, but in this case I only checked for Vosselman's 2014 thesis "book" linked above.

 

Edited by Sibiriak

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