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Saturated and Simple Sugars Cause Hypothalmus Damage and Obesity?

Blog Forums Nutrition Saturated and Simple Sugars Cause Hypothalmus Damage and Obesity?

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    The Real Amy

    Matt, did you see this article in Forbes?

    It claims that saturated fat and simple sugars cause longterm inflammatory damage to the hypothalmus leading to obesity in the long run. Thoughts? I haven’t read the whole study yet and it partly seems like a drug ad, but still it sounds a bit alarming!


    Hey Amy, I haven’t read this article but I’d like to comment, if you don’t mind. I do believe, after years of reading, that sugar definitely contributes to inflammation, but saturated fat is so important to the body, that I would seriously doubt any single study that showed it was harmful or inflammatory. In fact, they say it probably helps decrease inflammation due to stabilizing the unsaturated fats in the body and keeping them from oxidizing as much. Anyway, just my two cents =)


    I’d guess the study was based on CAFO beef as the source of saturated fat – which is a high Omega 6 variety, and yes, inflammatory.

    Grass fed animal fats have more Omega 3’s, which are anti-inflammatory.

    Omega 6:3 ratios:
    Grain-fed beef = 20:1
    Grass-fed beef = 1:6



    I wanted to share a few thoughts on this study and others like it.

    Here is a link to the whole article for those who have access (I do; in fact, I would attach the whole article if this forum could allow attachments, hint hint!)

    Stephan Guyenet posted something similar coming out of his lab a while ago:

    Fructose-Containing Carbs:

    My overview of the articles is that fructose and sucrose, in rats and in concentrations over 20% of the diet, stimulate a variety of inflammatory mediators that leads to liver damage and hypothalamic damage which can result in long-term set point dysregulations. According to the papers, glucose at any concentrations does not do this. From my reading, these manifestations are consistent with endotoxemia (mild ‘sepsis’) that result from fructose being malabsorbed and fermented into junk by gut bacteria/fungus/whatever.

    Antibiotics given with the fructose prevents the liver injury.

    In healthy humans, fructose is completely absorbed without problematic fermentation PROVIDED THAT the fructose is ingested CONCOMITANTLY WITH equal amounts of glucose. Glucose somehow facilitates the speedy absorption of fructose. In humans, sucrose (50:50 glucose:fructose) up to 100 grams or so in one sitting appear to be fine.

    Again, though, this was in ‘healthy humans’. This is consistent with the rat studies that show up to 10% sucrose is ok (5% fructose) and does not lead to any problems. Considering that most of these studies used 60% fat diets, this would mean about > 3:1 ratio of glucose:fructose. Thus, fruit and honey and natural things that contain roughly equal parts fructose and glucose would be fine for most healthy people, while particularly unhealthy people may want to have even more glucose and less fructose.

    Dietary ‘Saturated Fat’:

    After reading the papers over very carefully, I see ZERO discussion of ‘saturated fat’ outside of the conclusion, and all the trials were given up to 60% TOTAL FAT. The studies are showing that 60% fat diets can injure the brain and lead to obesity and diabetes compared to ‘control’ diets that are low fat and low fructose (high starch). Separate studies (summarized within the same papers) show that high fat diets (or medium fat diets) that are supplemented with EPA and DHA from fish oil (so, high Omega-3 PUFA, NOT omega-6 PUFA or miscellaneous PUFA) increase neurogenesis and thereby partially correct for the brain destruction from the high fat and/or high fructose diets.

    These conclusions in the paper are appalling to me since they didn’t take into account the fact that the base composition of the fat (whether ‘High Fat’ or otherwise) are predominantly high PUFA lard and high PUFA vege oils.

    As Masterjohn wrote a while back, the specific ‘High Fat’ diet used in most of these injurious diets was >30% PUFA (>50% of the fat was PUFA), with almost all the PUFA coming from linoleic acid (18:2, omega 6; the same major fatty acid as in soybean or corn oil).

    Masterjohn has actually eloquently written about this many times before, including in his article ‘Good Lard, Bad Lard’, but the site is down for me at the moment.

    This diet is often referred to as ‘High Saturated Fat’, but this is another example of researchers just flat-out lying to make a headline.

    So, back to the hypothalamic injury: we see that high fat diets WHEN THEY ARE HIGH IN LINOLEIC ACID, destroy the brain (and many other things), but decreasing this and adding fish oil somewhat counters this effect. All this proves is that omega 3 deficiency destroys the brain, and that high linoeic acid diets lead to omega 3 deficiency.

    IN SUMMARY, what is being claimed is that high sugar and high fat/saturated fat diets are injurious. In reality, the data actually shows that high fructose/sucrose and/or high vege oil diets are injurious. The vege oil thing we already knew. The fructose/sucrose thing I think is, AT THIS TIME, equivocal, but LIKELY IN MY ESTIMATE attributable to fructose malabsorption, which is a problem of fructose in excess of glucose–something much more likely with synthetic sweeteners and less likely with fruit, honey, and even cane sugar.


    Some very good info and points you made, Celtic! Thanks for taking the time to read and post all that =)


    Thanks, Jman99! I thank you for stating your appreciation :)

    But I wanted to both edit one of my comments above and clarify a couple things.

    First, I’d like to edit my comment of the PUFA% in my previous post. I mis-stated the amount of PUFA above in the High Fat Diet.

    I said the FAT CONTENT was >50% PUFA and so the TOTAL DIET was >30% PUFA. I mis-read this. The real numbers are that the FAT CONTENT is >30% PUFA, and so the TOTAL DIET is ~20% PUFA. Most of this is Linoelic acid, as I stated before. The ‘Scholarly Review’ looks at several trials, but the ones showing injury are using ‘lard’ which is now >30% PUFA. Once-upon-a-time, industrial lard was lower in PUFA and higher in saturated fat. That day is past.

    Second, my friend who reads this blog (and my post here) but does not comment asked me in person about my post, and I wanted to clarify something by highlighting a couple sentences from the original Review abstract:

    Quotes From Original Abstract

    1. Excessive intake of certain macronutrients, such as simple carbohydrates and SFA, can lead to obesity and attendant metabolic dysfunction, also reflected in alterations in structural plasticity, and, intriguingly, neurogenesis, in some of these brain regions.

    2. The present review draws together these observations and investigates whether PUFA may exert their attenuating effects on body weight through the stimulation of adult neurogenesis.

    3. Exploration of the effects of nutraceuticals on neurogenic brain regions may encourage the development of new rational therapies in the fight against obesity.

    My explanations:

    1. By ‘SFA’ (saturated fatty acids), the authors mean diets high in lard from pigs fed soybeans and corn, which results in fat that is ~30% Linoleic acid, with a n6:n3 ratio of about 17. The Saturated Fat content of the High Fat Diet appears to be about 30%, or about 20% of total calories in the overall High Fat Diet.

    2. By ‘PUFA’ (polyunsaturated fatty acids), the authors mean fish oils, with both EPA/DHA and straight DHA preparations used in various experiments resulting in the same result: attenuating (lessening) the damage of the High Fat Diet (the diet which, in reality, is high in linoleic acid n6)

    3. As The Real Amy said, these authors clearly have the goal of patenting/selling a drug/supplement/protocol which, though the norm in medical research, strongly biases both the questions and answers of the analysis.

    • This reply was modified 8 years, 7 months ago by celticphoenix.

    I came across this article somewhat by chance this morning.

    “Fat to treat fat: Emerging relationship between dietary PUFA, endocannabinoids, and obesity”

    It is another group of authors reviewing the literature on ‘PUFA’ (in this case, meaning both n6 and n3 PUFA) leading to the same abnormalities in endocannabinoids and inflammatory markers that the articles brought up at the beginning of this post sequence claimed were caused by ‘SFA’ (high PUFA lard).

    These authors, too, claim that fish oils can partially reverse the destruction caused by n6 PUFA.

    My point here is that data is now piling on that overall PUFA, especially perhaps vege oil PUFA, is THE leading cause of our obesity epidemic. And, of course, our anorexic tendencies don’t help either. For those people who have stated that eating to raise the metabolism DOES NOT fix the metabolic rate in everyone, and that it only further fattens people who are perhaps more ‘prone’ to obesity, I would say: here’s the next thing to focus on! Keep PUFA LOW!

    This article says something very instructive: modulating tissue and blood ratios of fatty acids (for the sake of example, ‘drowning out’ tissue PUFA with low to moderate overall dietary fat with a high overall percentage of saturated fat and low overall percentage of PUFA) REVERSES the biochemical markers associated with the obesity pathology. I suppose this is a verification of the anecdotal report that eating coconut oil ON TOP OF a routine diet leads to weight loss.


    Great find!
    Thank you for posting!!

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