I love your channel but I'm disappointed that you did not include research on nattokinase around its ability to remove arterial plaque. Also, berberine has been shown to remove arterial plaque. These are very important supplements to help people who can't exercise due to physical limitations or simply to help people who really struggle to get in shape. Many supplements can help people have an advantage until they can reshape all the other lifestyle factors needed for optimal health. They just give you an advantage even if you are healthy but you're older.

@@brianwnc8168 The evidence that berberine removes plaque is very early and needs more research - double blinded, case controlled study with enough participants. I do take it for that reason and it also does seems to lower blood sugar, BUT the only reason I take it without more evidence is that it does not seem to do any harm. So, I am hoping we eventually do get more robust/solid data. Nattokinase - not sure the evidence is there ... can you point me to some high quality studies? I AM SURPRISED HE LEFT OUT CREATINE MONOHYDRATE.

New subscriber. Just found your channel. Love it!🙂

Thanks, Mark

I second this.

I third this.

He’s buying the lipid hypothesis, but hiding behind “one of the contributors…”, otherwise excellent summary.

A minority also thinks that males can be females, and females can be males. So take that with a grain of soy😂

I've been taking glynac since last summer and taurine since the fall and I must say it has vastly improved my energy levels and I think it's actually improving the speed of my thinking, no small feat, despite being under 50. I also think NAC generally acts as a detoxifier which is beneficial.

I have a 95 year old aunt who I am going to try this on.

let us know your anecdote @@SkyRiver1

​@@SkyRiver1 Please let us know how it goes! Well wishes!

MDMA works wonders on pensioners too.

Gil is awesome. Humbled to be in his company.

You should only get diet advice from a real Ph.D in nutritional biochemistry with awards and honors and or a Nobel Prize with a long term track record of being right such as Roger J. Williams, Frederick Gowland Hopkins, Fred Kummerow, George H. Whipple, William Parry Murphy, Edward Adelbert Doisy. All 6 would say the same that Linus Pauling said that meat, poultry, fish and eggs are good for you in moderation and that dairy is ok in small amounts if you like it and are not allergic to it. Gil Carvalho has zero experience in anything.

Thank you for this. When you take this ? During or after meal ?

So you are now less bothered by critical thoughts about yourself and the world, past and future?

@@shahzamanhaque I try to take it on an empty stomach. I usually take a NOW 1G NAC pill with a glass of water mixed with glycine powder. Lately I have added 3 grams of Taurine to the mix as well as 2.5 grams of creatine.

@@oolala53 I think what the glycine/nac combination did for me was end the constant exhaustion, depression and edginess I experienced every moment of every day. It has given me space to work on the critical thoughts and destructive thinking patterns. Self enquiry and meditation have been extremely useful. anything that brings circulation to the prefrontal cortex. I really like the meditation devices like the Muse 2 and the Mendi.

Thanks so much for the kind words, Richard. :)

Hope things are going well on your end. :)

Toss in taurine and creatine monohydrate.

By day two of a water fast you will feel HGH in your body. So if you can do a 3 to 5 day water fast you will generate your own HGH. In my opinion the most efficient way to maximize water fasting is 7 days but it's not easy for a lot of people. The key here is that when you come off of the water fast your body will make up for the protein deficit by maximizing efficiency and rebuilding once you start adding protein as it leverages the HGH that was used to preserve muscle mass during the fast to build up even further; it might be 3 days of water fasting @ a minimum to see the HGH effect, I don't usually pay attention until I start feeling it in the morning and that's not until I'm already well into the fast.

I am going to check you on the TMG, but thanks in advance for the info if it checks out.

The thing is can you produce any HGH when you're 50+ ? or Testosterone ? No... not really, the charts crash badly. You produce very little, there's not much to stimulate "naturally". You have to supplement.

@@pavman42how does one feel HGH?

And boron

Nattokinase can do that

Because it's high in k2, right? I've heard it is not tasty 😂

I think it really depends. I can see the point in not eating for a long time as kind of exercise in restraint. But I lost 20 kg last year with frequent small meals. Often just a protein shake as snack at work. I feel that helped shrink down my stomach making me feel full being less full. Couldn't have happened with Giant 1-2 meals

How many grams per day do you use?

@@littlevoice_11 Initially I bought 600mg capsules and I had 1 in the morning and 1 in the evening. Now I have them as 400mg, and still trying 1 morning and 1 evening. I'm usually giving it a little break every 2 week cycle. 2 days off it every 2 weeks for now. I'm thinking of 3 times a day at the moment.

Well, if you’re subjectively feeling a difference it’s likely you were previously deficient…specifically with vitamin supplementation. Creatine is a totally different animal and can likely end up pushing the upper-bound ceilings of both skeletal muscle and cognition through tissue perfusion above supraphysiological states. NAD+ can be lower post infection, from chronic inflammation or stress, etc, so rebalancing that with supplementation may help with energy levels there.

​@@ilevitatecs2are you a doctor?

@@djurius I work in the research field but I do not have a postdoc

No buzz on my system.

Soothe2 / Supertone / Adobe Podcast / DXrevivePro 2 could work too in post production / while recording :)

That's for the physionic Insiders... to decode the secret message.

De rien, Pierre.

3 gm/day(min)

Found this: LDL cholesterol still a problem in old age? A Mendelian randomization study. Iris Postmus, Joris Deelen, Sanaz Sedaghat, Stella Trompet, Anton J M de Craen, Bastiaan T Heijmans, Oscar H Franco, Albert Hofman, Abbas Dehghan, P Eline Slagboom, Rudi G J Westendorp, J Wouter Jukema Author Information PMID: 25855712 DOI: 10.1093/ije/dyv031 BACKGROUND: Observational studies in older subjects have shown no or inverse associations between cholesterol levels and mortality. However, in old age plasma low-density lipoprotein cholesterol (LDL-C) may not reflect the lifetime level due to reverse causality, and hence the risk may be underestimated. In the current study, we used an LDL genetic risk score (GRS) to overcome this problem. METHODS: A weighted GRS was created using 51 single nucleotide polymorphisms associated with LDL-C levels. The LDL GRS was calculated in three Dutch cohorts: the Leiden Longevity Study (LLS) (n = 3270), the Leiden 85-plus study (n = 316) and the Rotterdam Study (n = 4035). We assessed the association between the LDL GRS and LDL-C levels, chronological age, familial longevity and mortality. RESULTS: Up to 90 years of age, in each age stratum individuals with high LDL GRS had higher LDL-C levels (P = 0.010 to P = 1.1 x 10(-16)). The frequency of LDL-increasing alleles decreased with increasing age [β = -0.021 (SE = 0.01) per year, P = 0.018]. Moreover, individuals with a genetic predisposition for longevity had significantly lower LDL GRS compared with age-matched individuals of the general population [LLS nonagenarians vs > 90 years: β = 0.73 (SE = 0.33), P = 0.029, LLS offspring vs partners: β = 0.66 (SE = 0.23), P = 0.005]. In longitudinal analysis, high GRS was associated with increased all-cause mortality in individuals > 90 years, with a 13% increased risk in individuals with the highest LDL GRS (P-trend = 0.043). CONCLUSION: Results of the current study indicate that a genetic predisposition to high LDL-C levels contributes to mortality throughout life, including in the oldest old, and a beneficial LDL genetic risk profile is associated with familial longevity.

Could be, Ken. I'm not convinced, yet, but I'm open to the idea.

I cover funding in my analyses. I agree that funding is important, but it's often overblown in importance as if it is *the* deciding factor to believe or not believe a study, and I disagree with that notion.

I’m on it. 3 months of work. I expect the video to release in 2 weeks.

I’ll be counting down the days. Thanks so much. Just for your info, I’ve been taking niacin in large doses (1000mg) and it has dropped my Lp(a) significantly. But of course I can’t be sure that lowering it alone will actually reduce my risk of atherosclerosis.

Agreed with the slight amendment to "ldl -c is not the best predictor of CVD risk, but often correlates pretty well with apo-B". Total Ldl not great but a very high level should be a red flag which merits further investigation - see below. apo-B represents the measured particle concentration of VLDL, IDL, LDL and chylomicrons (unless lipid panel done on a fasted state in which case less of an issue). Whereas LDL-c is an estimated/calculated representation of the amount/volume of LDL-c in the above particles. For most people, apo-B and LDL-C correlate well. But for a significant minority there is discordance - with High apo-B/low LDL-c or low apo-B and high LDL-c. For all these cases, study after study has found that it is the apo-B level which is the greater predictor of heart disease. Does this mean we should ignore LDL-c? No. If high for example, there is an odds on chance that apo-B will also be high. Some individuals will jump on the "low LDL-c and still had heart disease" so called paradox. But two possible explanations: 1) As above, could be discordant and have high apo-B or 2) Reverse causation - where CVD events (including deaths where blood panel measured post-mortem) show low LDL-c. In these cases it is the event/chronic illness itself which lowers LDL-c at the point of measurement. Hence the U shaped curve for risk vs LDL-c. Conclusion - LDL-c is not irrelevant but is a poor man's surrogate for apo-B which is the better predictive risk factor. Interestingly, in the UK, for some years the lipid panel now includes "Non-HDL cholesterol", which is not perfect by any means but correlates more strongly with apo-B than LDL-c alone. Finally, for me it seems that it is the apo-B concentration over a lifetime that counts (the area under the curve). I have seen some great explanations for this by Dr Thomas Dayspring (good interviews with Simon Hill - The Proof), Peter Attia and Dr Gil Carvalho of Nutritionmadesimple. Their mantra for apo-B is lower, earlier, for longer. Disclaimer: while I have some background in Chemistry (not Biochemistry) I don't claim to have any specialist knowledge of lipids, CVD risk etc etc. I'm just trying to read and learn from a very low base - my apologies if I've got some of the above mangled!

Nope! Debunked. Total ldl is a great predictor of atherosclerotic heart disease and death