The world at large will never be convinced of the benefits of low-carbohydrate diets until the still-vilified "saturated fat" is fully acquitted of the charges falsely laid in the courts of public opinion. Butter is the poster child for the defendant saturated fat, and also the most nutritious and beneficial of the all-fat foods. So any campaign to vindicate SaFAs should begin with butter.
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Pharmacological studies and siRNA knockdown experiments showed that NaB-mediated AMPK activation induced the phosphorylation and nuclear translocation of Sirtuin 1, leading to the increased assembly of mammalian TOR complex 2 and phosphorylation of AKT at Ser473 and subsequent induction of Nrf2 expression and activation. These favorable changes caused an obvious decrease in hepatic fibrous deposition, GST-P-positive foci development, and hepatocarcinogenesis.
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If anyone needs reminding why it is essential that very low carb diets enter the medical mainstream today rather than tomorrow, I recommend Toxic's post on the subject. This is incendiary stuff, and if it doesn't make you feel like fire-bombing a bakery you have no soul.![Churn, butter; Henderson & Pollard Ltd; [?]; CT78.743]()
![Churn, butter; Henderson & Pollard Ltd; [?]; CT78.743](http://f1.ehive.com/3021/1/6ghj9o_127i_m.jpg)
(Minimal processing is required - you can make butter from cream at home with a jam jar and a marble)
A few weeks or months back I linked to the two studies by Mozaffarian et al. showing a protective association between dairy fat and diabetes (2010 and 2013). I pointed out that these observational studies used a more reliable measurement than the food frequency questionnaire, and that the correlation was of an order of magnitude (0.38 and 0.52) significant enough to be meaningful in the presence of plausible mechanisms. I know that some bloggers tend to completely reject dietary epidemiology, understandably given the mistaken weight given to the weakest correlations by prejudiced scientists in the media, but strong correlations imply causation, and will constitute part of the proof if causation is considered proven. Professor Feinman has written an excellent guide for the perplexed on the value of epidemiological studies in the scientific tradition, which I recommend to anyone confused about the issue.
Back when I was really sick with hepatitis and food allergies and so on, I thought I didn't tolerate fat so well. Fatty foods like icecream or creamy desserts made me throw up, and given the advice one heard, and still hears, the fat seemed the obvious culprit. But I could always eat butter without any problems, and I found it interesting that this fat, which I knew to be highly saturated, should never make me ill, indeed seemed to make me feel better. But still I took seriously, and to my shame repeated, that pernicious meme about saturated fats being bad and vegetable oils beneficial. It's called cognitive dissonance. Until one day in a spirit of inquiry - and thank God for the internet - I googled "health benefits of saturated fats", came across Mary Enig's writing on the Weston A. Price website, checked out the references, and came away a new man.
What is the fat in butter? It's the fat produced from a 100% plant-based, high-fibre diet by an animal actually designed to eat one. It's what cellulose would become in our bodies if we (or rather our microbiota) could metabolise cellulose, plus the products of other fibres, starches and sugars in the grass, silage, or other feeds, and any fatty acids therein. One of these products of fermentation is butyric acid, incorprated in triglycerides as butyrate; butyrate makes up 3-4% of butter and is also formed in the human gut when dietary fibre is fermented by the right bacteria. Most of the benefits of fibre in the diet seem to relate to the formation of butyrate, and if the bacterial species present are those that instead prefer to generate D-lactate, or high levels of propionate, the results will not be beneficial - see the section "D-lactic and propionic acid - a cautionary tale" half-way down this probiotic review.
What is the fat in butter? It's the fat produced from a 100% plant-based, high-fibre diet by an animal actually designed to eat one. It's what cellulose would become in our bodies if we (or rather our microbiota) could metabolise cellulose, plus the products of other fibres, starches and sugars in the grass, silage, or other feeds, and any fatty acids therein. One of these products of fermentation is butyric acid, incorprated in triglycerides as butyrate; butyrate makes up 3-4% of butter and is also formed in the human gut when dietary fibre is fermented by the right bacteria. Most of the benefits of fibre in the diet seem to relate to the formation of butyrate, and if the bacterial species present are those that instead prefer to generate D-lactate, or high levels of propionate, the results will not be beneficial - see the section "D-lactic and propionic acid - a cautionary tale" half-way down this probiotic review.
(Sheep's milk is higher in butyrate and MCTs than cow's milk)
A popular probiotic in Japan is clostridium butyricum, which generates high levels of butyrate from dietary fibre. It turns out that these probiotics, or the butyrate derived from them, protect the liver from cirrhosis and cancer in the rat model of fatty liver disease (a diet deficient in choline and methionine - eat your eggs folks! Another demonized food that can actually save your life. In Colin T. Cambell's contentious China Study, the raw data shows a significant liver-protective effect of egg consumption). This study is a treat, full of photos and easy-to-understand graphics. It shows that even in the choline-methionine deficient rat (a huge metabolic barrier to surmount) the progression of cirrhosis and cancer is significantly slowed by butyrate (NaB).
Pharmacological studies and siRNA knockdown experiments showed that NaB-mediated AMPK activation induced the phosphorylation and nuclear translocation of Sirtuin 1, leading to the increased assembly of mammalian TOR complex 2 and phosphorylation of AKT at Ser473 and subsequent induction of Nrf2 expression and activation. These favorable changes caused an obvious decrease in hepatic fibrous deposition, GST-P-positive foci development, and hepatocarcinogenesis.
100 grams of butter, which would be about 1/3 of a day's calories, will supply 3-4 grams of butyrate and this is (roughly) as much as 6-8 grams of dietary fibre will supply under perfect conditions. The RDA says that foods that contain more than 6g fibre per 100g are considered high fibre foods, which means that butter is, in effect, a high fibre food, one where there is no risk of the fibre going to feed the wrong bacteria - it's all good. Cook some greens or other fibrous vegetables with your butter if you like, it helps to keep it on your knife, as when eating peas with honey.
(Camel's milk is the most hepatoprotective milk there is)
Here's an interesting human study showing that fat is the most important nutrient for people recovering from hepatocellular cancer (PDF). It's been couched in some technical oncologist or biophysics jargon that is mildly impenetrable, but what I get from it is this: people with cirrhosis do worse if they don't get enough energy (this is a universal finding - non-alcohol calories protect against cirrhosis progression). They tend to undereat protein, but the deficiency that has most impact on cancer recovery is fat. And the reason for this is that the metabolically damaged cirrhotic liver cannot derive energy from carbohydrate and protein with the same efficiency that it can generate ATP from fat. I can think of two reasons; a damaged liver has difficulty synthesizing co-enzymes from vitamin precursors, and the generation of ATP from carbohydrate and protein requires more variety of co-enzymes to be synthesized, and more enzymes, than the relatively simple, repetitive process of fatty acid beta-oxidation. The other reason will be familiar to regular readers of Hyperlipid; if the mitochondrial damage is mainly at Complex I, as is almost always the case for some reason, this will impede the generation of ATP from glucose (more NADH, less FADH2 generated, complex 1 handles the NADH) more than it impedes generation of ATP from fat (more FADH2 relative to NADH).
Fat, therefore, is easy on the liver, and saturated fat the easiest of all, because the simplest to metabolize. I've shown in earlier posts how saturated (and monounsaturated) fats protect the liver because of their inherent stability compared to polyunsaturated fats, passively supporting the liver's antioxidant defenses. Butter also contains fats as MCTs, up to 15%, less than coconut oil, it's a source of vitamins A, D, E, and K2 as well as carotenoids, cholesterol and CLA. I'm sure there's another post in all this, but I've written more than enough already.
Fat, therefore, is easy on the liver, and saturated fat the easiest of all, because the simplest to metabolize. I've shown in earlier posts how saturated (and monounsaturated) fats protect the liver because of their inherent stability compared to polyunsaturated fats, passively supporting the liver's antioxidant defenses. Butter also contains fats as MCTs, up to 15%, less than coconut oil, it's a source of vitamins A, D, E, and K2 as well as carotenoids, cholesterol and CLA. I'm sure there's another post in all this, but I've written more than enough already.