Is Longevity Related to the Suppression of Endogenous Fructose Production?
I didn’t even realize that The Vicious Cycle of Obesity could be quite a good explanation for commenting on the results of an interesting longevity study. On X, an innocent question appeared:
Quote
Someone needs to explain this.
"In total, 1224 participants lived to their 100th birthday"
Higher levels of total cholesterol and iron and lower levels of glucose, creatinine, uric acid, aspartate aminotransferase, gamma-glutamyl transferase, alkaline phosphatase, lactate dehydrogenase, and total iron-binding capacity were associated with reaching 100 years.
End of quote
What is the author of the question getting at?
At the results of an interesting Swedish study, in which the authors sought to describe and compare the biomarker profiles of people between the ages of 64 and 99 who eventually became centenarians, with their peers who did not reach 100 years of age. They examined how homogeneous the biomarker profiles of centenarians were earlier in life. For this, they used data from the AMORIS population cohort, which contains information on blood biomarkers measured between 1985 and 1996, spanning up to 35 years. They analyzed biomarkers of metabolism, inflammation, liver, kidneys, anemia, and nutritional status. A total of 1,224 participants (84.6% women) lived to their 100th birthday.
Take a look at the published results yourself.
What do we see here? On the horizontal axis is the risk factor for reaching 100 years. The further left, the lower the chance of survival. The further right, the greater the likelihood of longevity. The rows are divided into groups tracking a single marker in five different levels. For each level, the probability of reaching 100 years is evaluated separately. You can therefore see for yourself what is risky and what isn’t. For instance, a fasting glucose level of 6.0 mmol/L (108 mg/dl) or higher reduces the probability of reaching 100 years to 0.67, that is, by 33%. But a level of 5.3 mmol/L (95 mg/dl) or lower does not shorten lifespan. Interesting, isn’t it?
Let’s go further. The first marker listed is TC (Total Cholesterol). Cholesterol has no effect on reaching 100 years unless we note that too low total cholesterol — that is, 5.2 mmol/L (200 mg/dl) or less — reduces the probability of living to 100 by about 20%. So maybe it’s not the most important indicator of population health after all? Uh-oh! That must be some kind of system error, right? Or is it really true? Maybe the numbers don’t lie!
For me, perhaps the most interesting marker is uric acid, because it appears as a product of xanthine oxidase (XO) in the vicious cycle of obesity, as I mentioned in previous posts. We can see that the dependence of the probability of reaching 100 years on uric acid levels is inverse and almost linear. The lower the uric acid in the blood, the longer the life? It seems so.
Does this mean I’m on the right track? The longevity study confirms that uric acid production is closely linked to the risk of shortened lifespan. But now we get to the question—why? Where does it come from? How can we influence uric acid formation? But we know that. It comes from purines, from AMP, from adenosine and inosine. It’s fructose that activates the AMPD2/XO/UA pathway, i.e., uric acid production.
Most people would now say: “I just won’t eat sugar that contains 50% fructose, and I’ll live a long life.” This attitude ignores the fact that in the liver, everyone can produce fructose on their own, without eating any sugar, fruit, or honey. This is due to the polyol enzymatic pathway. And as I explained earlier, this pathway also breaks down toxic products formed from linoleic acid through its peroxidation into aldehydes during oxidative stress. This leads to much greater activation of the polyol pathway than in the absence of these toxins. Perhaps other toxins can also activate the polyol pathway—I don’t know yet. It would be good to investigate that.
In any case, explaining uric acid production through endogenous fructose still seems the most likely to me. While we’ve always encountered fructose in fruit and honey since ancient times, omega-6 polyunsaturated fats have never been as abundant in our diet as they are today (industrially produced seed oils, or even fat from animals fed oily seeds). Their effects are long-term—they must first be incorporated into cell membranes, and only then, under oxidative stress, do they begin producing more toxic aldehydes that activate the enzyme aldose reductase (AR) in the liver and stimulate endogenous fructose production. At the same time, this means that it won’t be easy to flush linoleic acid from the body; it takes years, even with zero intake. I have already written about this as well.
But we don’t need to despair and think there’s nothing we can do. That our bodies are already full of linoleic acid. Fortunately, there are ways to compensate for or suppress the effects of endogenous fructose. Yes, for example, vinegar/acetate. You can find more in earlier posts. What’s very important is that vinegar/sodium acetate does not suppress the detoxification function of the polyol pathway; it only compensates for the negative effects of fructose. It therefore does not slow the body’s cleansing from linoleic acid. So let’s give it a try—let’s live to be centenarian :-)
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