I Read 250 Studies: 10 Things I Learned about your Health

• Analyzed 150 studies along with 100 from the previous year
• Insights on influential health findings shared
• Personal interpretations clarified
• Research on health supplements and their effects discussed
• Emphasis on the importance of data from multiple sources

I've spent the last year analyzing 150 studies to add to the 100 studies that I analyzed the previous year. I've written notes on every study. I've made videos including each study, and I've read far more than these 250, but for a trackable count, we'll stick to these 250.

So what have I learned about our health? Well, I'll cut through the science and tell you 10 of the most influential and interesting before we begin. Like I said, I've made videos on all these, so I'm going to post the study number on screen so that you can search for it on the channel using the study number and the word physionic. That said, I'll also post what videos I can below for your convenience. Enough housekeeping. Let’s get into it.

Number one: GLC GLINAC is a combination of the molecule N acetylcysteine and the molecule glycine. There have been a few studies looking at them in combination, thereby being abbreviated as glyc. I covered three studies on one in animals showing remarkable results and another two in humans also showing remarkable results. GLINAC allows the production of glutathione, a potent endogenous or within our cells produced antioxidant molecule. Anyway, these few studies showed glyac had tremendous effects against insulin resistance, markers of DNA damage, mobility and much more, which certainly got me excited.

Now, I don't take GLYC because it beat me up when I was a kid and I'm holding a grudge. That or the studies were only done in people in their 60s and 70s, and considering my antioxidant capacity is likely still quite high, it seems unlikely to be a benefit for me.

And there's even a tiny bit of evidence corroborating that train of thought. Now, last time I said that, a lot of people got upset with me because they thought that I was basing my interpretation of the GLINAC data on how it would apply to me. I literally never do that. I always base interpretations of the data and how it applies to the population, aka you, even if I share my personal choices from time to time.

So since physionic is involved in the game of nuance one year later, I haven't seen anything that changes my mind on the supplement. So here's my interpretation: If you are healthy and aged below 40 or 50, Glinac is unlikely to be a huge benefit for you. However, if you're approaching your 60s and beyond, Glinac may provide a significant benefit. It may also be beneficial for those that are under 50 and are troubled by certain health conditions.

Additionally, there's still very little stu on the topic, more on N acetylcysteine and much less on GLINAC in combination. And since all these data come from one laboratory, I would still like to see more data from independent sources. I remain steadfast and consistent on that stance until I see reason to change that stance. I know plenty of people have had great experiences, so feel free to share yours down below.

Number two: Collagen for Skin. I analyzed 11 studies for this sucker, and the results were relatively consistent in favor of collagen peptides for reversing signs of skin aging. Granted, not all of the studies were of the greatest quality, but across all 11 the evidence points in favor. If we look at just one piece of data, we can see a measure of eye wrinkle volume. The higher the worse; the dark bars are the placebo condition (so those that did not consume collagen) and the lighter bars are those who did consume collagen.

Clearly, the collagen condition seems to regress in wrinkle volume, although admittedly this statistical comparison was only against placebo, not baseline. I won't bore you with the details, but anyone with a stats background will understand. Still, this isn't an isolated study. Others showed similar results in favor of collagen supplementation.

Now that said, many of these studies were industry funded, but those studies that had no conflicts of interest found similar results to the industry funded ones. So interpret that as you will, but you know where I fall.

Number three: Omad on health. You would think there would be far more studies on omad, otherwise known as one meal a day, wherein you literally just eat one meal a day. But the studies are few and far between. I found four studies that I felt qualified. I have an in-depth study analysis of the studies for a complete breakdown. But here's the bottom line: omads seemed to be great for weight loss and likely improves a number of metrics of health, assuming that weight loss is achieved.

Interestingly, most of these studies tried to make sure that people did not lose weight, and when that happened, there was actually a slight worsening of glucose blood sugar tolerance. Now before you jump down my throat, I'm well aware that most people that adopt the Omad eating style lose weight, so there is low translation to the real world.

I also think that these studies suffered from a methodological flaw in that they told people to consume their one meal at the end of the day, and if you measure blood sugar and insulin after an overnight fast. Yet one group of people consumed all their food in one meal the night before, and the other consumed only one-third of their food that night before dinner because they were consuming breakfast and lunch.

To spread out their total intake, it seems reasonable that the OMAD group would be processing and digesting that food at the time of testing, unlike the non-OMAD classical food consumption group. Either way, you can learn more about that in that video.

Number four: Reversing aging. I covered a single incomplete study called the TRIM study. This study showed it is possible to reverse certain potent metrics of aging using a cocktail of molecules. I'll describe two incredible effects. One is related to an age related thymic involution. If you think I'm talking Klingon suddenly, don't worry, I'll explain what that is.

Your thymus is a tissue that is of high importance to your immune system. I won't go into the details here. I'll leave that for the full video that I made. However, what you should know is that your thymus, by the time you're 60 or so, will fill with fat tissue. Essentially, the active th DY cells get crowded out and replaced with adipocytes. Those are fat cells to eventually lead to the replacement of the entire thymus into a fat globule.

However, with this cocktail of molecules the researchers used on these people, the thymus reversed its fatty state back to its lean thymic state, or that's what was assumed, and some preliminary data did show that to be the case. From a cell biology perspective, this is incredible because for cells to return back to their functional state, it requires a massive genetic reprogramming of the cells.

I won't go into detail here again because of time, but it's a seriously cool phenomenon. The second thing that these researchers showed was the ability to reverse the participants' biological clock as measured across a variety of epigenetic experiments. Epigenetics being in simplistic terms, the tags that are placed or removed on our genes to either lead to the gene being read or expressed more or less as one piece of data.

You can see the difference in chronological age compared against biological age. The vertical axis is the amount of age difference between the chronological epigenetic ages. So if it goes into the negatives, that means there is a lower biological age compared to chronological age.

The horizontal axis is the amount of time on the treatment. The treatment was applied for 12 months and then stopped, so the measure at 18 months is six months without treatment. What you'll notice is that the difference between the beginning month 0 and 12 months there is an increase in the difference between the biological measure and the chronological age, indicating these people are, at least by these epigenetic measures, getting younger relative to their chronological age and not by weeks or months, but by years.

Additionally, the researchers pointed out that the age reversal sped up after the initial nine months, but the trial had to end at 12 months. So it would be fascinating to see what would happen after two years time or three years time, for example.

Also, notice that the effect persists after six months being off treatment, although it is possible that it is slowly returning to equilibrate with chronological age. Wickedly cool, but there are some caveats.

First, the study did not have a control group. It was a prospective single-arm intervention trial, so while fascinating and promising as well as unlikely to be a placebo effect, we can't be certain. The study was limited in its participants. It was a small study and only included men; those two primary critiques mentioned.

It should be noted that the study is being redone as a clinical trial, including women this time. So that will wrap up in about a year when this video releases. I'll be sure to cover it when it releases.

For those of you that waited until now, lean in real quick so that no one else can hear us. The molecules given were human growth hormone, DHEA, metformin, vitamin D and elemental zinc. My impression of the research is that HGH was the primary active ingredient, and the others were either there to facilitate the positive effects of HGH or mitigate the negative effects of HGH, like DHEA and metformin.

I get that it isn't the most affordable cocktail nor the easiest to get your hands on, but this is what the researchers used and found effective.

Number five: Being overweight encourages autophagy. Autophagy is one of those buzzwords that you'll hear a lot of influencers throw around in relation to fasting, particular supplements, particular diets, and so on, as if it's this definitively positive thing. However, what if I told you that having the opposite, being over fat, increases autophagy too?

Before you slap your forehead and yell, "Is science sure of anything these days?" The answer is yes. But influencers, pop science channels and charlatans do not speak for scientists. Always keep that in mind.

What makes me different? Well, I've been working in a lab for 10 years now and I've published studies on autophagy. Anyway, my little rant aside, all those influential habits that I mentioned before, fasting, supplements, etc. Can definitely increase autophagy. So rest easy, it's all true.

However, I went over five studies on the topic and it seems to be true. When taking tissue samples from obese individuals, we tend to have an elevated autophag marker. We can see that here.

We're looking at microscopy images of cells under a microscope. So the red fluorescence is a common protein involved in autophagy called LC3. And the two top images are the obese individuals and the bottom two images are from normal weight non-obese individuals. If you see red, you are likely seeing autophagy.

There are some nuances to that statement that an autophagy researcher might disagree with, but this data, including some other data, leans us in the direction of autophagy being elevated in overweight individuals.

Okay, so two outstanding questions remain. One, why? And two, is obesity healthy then? Well, one, the mechanisms for why are unknown, but there have been some speculations.

I'll leave most of it for my dedicated video on the topic. But one idea is that autophagy, or more so the autophagy machinery, is being co-opted for moving large chunks of material around the cell without actually degrading them. Another idea is that it is used to eliminate inflammatory cytokines.

Those are proteins that attract immune cells to reduce the inflammatory burden. Now, if you aren't familiar with autophagy, it's this mass degradation system within our cells. So these vesicles envelop organelles and proteins and other molecules within our cells and destroy them.

So the latter possibility is a strong one. However, there are other possibilities that I've discussed as well. As for the second question, the answer is a resounding no. Autophagy is often attributed to being a positive to our health, and it often is. But it doesn't mean it always is.

Nor does it mean that it is the only metric that we should aim for. Autophagy can be upregulated in an unhealthy scenario for a number of reasons, but the scenario can still be unhealthy, aka Obesity.

Number six: Insulin versus calories driving obesity. This has been a heated debate for some time. The heavy favorite for most scientists is to see calories as the primary reason for fat gain and fat loss. However, a vocal minority of researchers disagree, blaming the hormone insulin as the primary driver of fat gain.

Both sides have put forth many studies corroborating each side, and they've gone back and forth with one another in debate, which I covered in my dedicated video. In short, Dr. Hall, representing the calorie side of things, has been debating across multiple studies and commentaries with Dr. Ludwig, who represents the insulin model of obesity.

Remarkably, they've even come to some agreements after discussion, which is really fantastic to see. For example, one area of uneasy agreement is that a low insulin diet, meaning low carbohydrate, may provide a slight benefit to metabolism, increasing energy expenditure.

Both research groups analyze the same data and they both tentatively agreed that the effect might occur. However, the reason why I mentioned tentative is because the magnitude of the effect is portrayed as much greater in the Ludwig insulin camp and much smaller in the Hall calorie case.

It is also true that giving insulin without increasing calorie consumption does lead to more fat deposition. However, on the other hand, there's also evidence across many human studies that people can lose body fat on a very high carbohydrate high insulin diet. So what gives?

Ultimately, there's a ton to cover here because even those that believe in the established calorie model acknowledge advantages of low carbohydrates diets like greater potential satiety, better adherence, easier fat loss and such.

But their arguments aren't that low carbohydrate or low insulin diets are inferior, just that the conventional calorie model easily explains these results without needing to rely on insulin as the explanation.

If you want my opinion, I strongly believe the calorie model, but not based on some blind belief, but because I've analyzed at least 20 studies showing it to be true.

Additionally, deep diving into some of the corroborating insulin studies for the insulin model, they fail to exclude explanations brought up by the calorie model. Like I said, there's so much more to discuss here.

Number seven: Low Density Lipoproteins on Heart Disease. Low density lipoproteins, or LDL for short, are these particles in our blood that carry cholesterol molecules and triglycerides. These are fat molecules across the body, delivering these molecules to the cells of our body.

Conventional understanding of LDL particles is that they are too abundant in the blood. They can cross our blood vessel walls and get stuck because proteins called proteoglycans found in the blood vessel wall attract a protein found on the LDL particle called apob.

If there are high concentrations of blood LDL, more LDL gets trapped in the wall than leave the wall, eventually leading to this immune cell invading into the wall and consuming these trapped LDL. Unfortunately, this only worsens the situation as immune cells macrophages turn into dysfunctional cells called foam cells.

From there, the inflammatory cascade continues as more immune cells are attracted to the region to also eliminate these foam cells. But during this whole process, and as more LDL bind to the area, the wall pushes inward as the plaque formation of dead cells, dysfunctional cells and high LDL burden leads to a series of other events pushing the wall inward, creating shear stress on the wall, which could eventually lead to the rupture of the plaque and creating a blockage downstream.

Now, there has been a vocal minority of people who argue that LDL is causative to heart disease. While the majority of scientists and lipidologists are sure of LDL's plaque forming role, there's still a vocal social media presence, including some medical doctors that disagree.

Some of the arguments levied are that LDL is only an issue when it is glycated from high blood sugar, or it needs to be oxidized aka damaged or chemically altered, or that the blood vessel wall needs to be damaged first, or that this is only an issue in small dense LDL particles and not an issue in the larger, fluffier LDL particles.

After reviewing 17 studies publicly and reviewing many more privately, I'll offer these words. There is scientific evidence that LDL is one of several risk factors for heart disease, even with normal blood sugar, even when looking at less oxidized versions, even when the blood vessel wall is not damaged, and even with larger LDL particles.

Now, there have been a few studies looking at people who are lean and generally healthy, except that when they jump on a low carbohydrate diet they experience a sharp rise in LDL. This phenomenon has been dubbed the lean mass hyperponder, and it looks more and more that this may very well be a real phenomenon.

However, the evidence to date on this subgroup of individuals does not prove that LDL is not a heart disease risk factor, although it is often reported as such. This may change in the future as more convincing data releases on these lean mass hyperponders.

But as it stands, high LDL is one of several heart disease risk factors and 99% of scientists leading experts in the field, thousands of them, as well as the majority of studies and data, including many independently funded studies, are in agreement that high LDL is one of several risk factors for heart disease.

Number eight: Urolithana supplementation. Urolithina is a molecule produced by the microbes of our intestine. When we consume polyphenols, they get absorbed by these microbes and undergoing an enzymatic reaction, they produce urolithina. This molecule then traverses into our bloodstream and is then believed to help in mitochondrial health mitophagy, which is autophagy that we discussed earlier.

But for mitochondria specifically and some other indices of health, the exact mechanism is still unknown. But I went over all the human trials up to the point of this recording to see if urolithina supplementation actually helps.

If we crack open a little data, we see the effect on mitochondria. Here we're looking at gene expression across a multitude of mitochondria production genes. So the more of these genes, the general idea is that we’d be developing more mitochondria.

There's some scientific nuance that I won't go into, but the bottom line is urolithina had no effect. You might see some of these red bars are much larger than the others, but statistically speaking, there's no effect seen. The reason that the red bar is so large is because what is known as a wide standard error of the mean, thereby increasing the uncertainty of the analysis.

The bottom line is still urolithina has no effect. However, when the researchers extended their analysis to what is known as gene set enrichment analysis, including many more mitochondrial genes, they found some changes with urolithina supplementation.

So hopefully you can see why I wasn't exactly blown away by the results. Additionally, when we look at some of the other metrics, the effects were again either nonexistent or small, depending on what outcome that you looked at.

I actually covered several more for the physionic insiders, but either way nothing really jumped off the page. So that doesn't mean that urolithina is ineffective, just that it probably should be based on this limited data.

Further down on the list of priorities. Once more data releases, I'll update that stance, but as you can likely guess, you can learn more in my dedicated video linked for you.

Number nine: Fish Oil on cognition. Fish oil had been a popular supplement for some time. I think the primary focus has been on cardiovascular health. I haven't looked at that data so I can't speak to it yet.

However, I did go over seven studies on its supplementation for brain health and the idea is that since our brain is primarily made up of omega 3 polyunsaturated fats, docosahexaenoic acid or DHA for short, that having a steady stream of omega 3 in the blood allows the brain to import more for its health and maintenance.

Now, the focus of the analysis was on people with mild cognitive impairment, so not dementia, but dealing with some small cognitive deficits. In that analysis, it showed consistently that omega 3 supplementation, if that's fish oil or otherwise, does improve cognitive ability.

For example, if we look at some of the major indices of cognitive health, yes, a bunch of numbers, but it'll be easy to read, I promise. We can see four outcomes on the left side: memory, executive function, language and visio spatial effects. Then if we look at the standardized effect size known as the Hedges G which tells us how much of an effect Omega 3s had on these outcomes, we see four numbers, all less than one.

Without boring you with the numbers much longer, I'll just say that these effects are either minuscule or small. The greatest effect was on memory and the effect was small. So not earth-shattering results here, but if we're combating cognitive decline, even a small benefit from a supplement might be worthwhile.

Especially considering that we're looking at real-world outcomes, not something like, I don't know, more cellular, like increased autophagy. I have a lengthy multi-hour analysis of all these studies for you to look over everything for yourself.

And there's so much more to be said on this topic. But if you know someone potentially older with some mild memory deficits, it may be worthwhile to have them try an Omega 3 supplement with a focus on DHA. Don't expect a quick turnaround either because brain remodeling takes many months to a year or more. So it may need to be taken consistently at least a year to assess accurately.

Number ten: Reversing heart disease. I analyzed six studies for this topic, which is oddly controversial because some scientists do not believe that we can reverse atherosclerosis, which is the technical name for plaque buildup in our arteries. And the other scientists believe it is possible.

Well, I can tell you that in animal studies there is definitive mass recovery of the artery after dramatic atherosclerosis progression. That much is well known across a number of species. However, it doesn't seem to stop at other animals, but extends to humans as well.

I would like to see more studies on this topic to be certain. But the studies that I was able to find did show plaque reversal, like here. These are images of the lumen of the artery, the opening of the artery of three people. The top images are before and the bottom images are after intervention.

You can clearly see that the artery opens up more for at least two of the three individuals. However, these are isolated images, so they should be interpreted with caution.

That said, there's more than just these images. And the averaged data from a number of measurements across multiple studies show improvements in atherosclerosis progression. Now what did they do? Well, they did the simple things. They exercised, they changed their nutrition, they lost body weight, and there was an association with a reduced blood pressure as well.

It wasn't supplements, it wasn't quick fixes, it was dedicated lifestyle changes. As more data comes out, we'll be able to get more granularity on which diets, which exercises, and potentially which supplements and other molecules might help with this process. So I expect to keep my eye on this topic for the future.

You know where to find more details, the links. But before you do that, I did cover 10 lessons learned from 250 studies. However, in truth, it was 10 lessons from 150 studies because the previous 100 studies that I analyzed were covered in this video right here of 10 more things that I learned. If you enjoyed this, you'll enjoy that one. I'll speak with you there. Bye.