The other day I rediscovered one of my early posts about my concept of a high fat diet for Hep C.
It was posted on the Life Extension Foundation forum on 27 Feb 2011.
I started restricting carbs after reading "Protein Power" by Michael and Mary Eades, where the rationale for reducing inflammation by restricting carbs and eating more fats is spelled out.
This was good, but it wasn't till I read "Dr Atkin's New Diet Revolution" that I saw the link between what happens to VLDL/TG on ketogenic diets, and what HCV does to exploit lipids.
Next, I found out about the Nanji-French research that demostrates a liver-protective role for saturated fat, and tried limiting PUFA.
Then (about October 2010) I started to get the results I wanted and was ready to write about it, so I posted about it on MySpace (remember MySpace? Tom you bastard, I want my customized settings back!) then posted this at LEF (to date there have been no responses).
http://ask.lef.org/1620/Atkins-Paleo-Diet-for-treatment-of-Hepatitis-C?keywords=DIET&pageindex=1
the HCV virus
is linked exclusively to lipid metabolism (blood fats, commonly but
erroneously called "cholesterol").
- HCV virion is completed by enzyme DGAT, which also packages fats
(triglycerides) prepared by the liver.
- HCV virion escapes infected liver cells via VLDL-c expression.
VLDL-c (very low density lipoprotein cholesterol) carries fats made by
the liver to cells that need them, also carries cholesterol and
lecithins made by the liver.
- HCV virion enters uninfected liver cells via LDL-c receptor. LDL-c
is remains of VLDL-c after fats have been delivered. The fewer
triglycerides, the larger the VLDL-c and LDL-c, hence the fewer interactions there will be with receptors.
This is why HCV only infects the liver - only hepatocytes have all of
these enzymes and receptors.
Now, where do triglycerides and VLDL-c come from? Over half comes from
the carbohydrate in the modern high-carbohydrate diet, converted to
fats for storage or energy, and this half is not produced at all on
high-fat diets.
In other words, on a high-fat, very-low-carb diet, serum levels of
triglycerides (FAT = Fatty Acid Triglycerides) and VLDL-c are
approximately 50% of the levels seen on a low-fat diet.
This diet should automatically reduce the HCV viral load by a similar
amount and the reduction should continue over time. Because the LDL-c
receptor is upregulated on the high-fat diet, probably increasing
uptake of HCV (yet the LDL-c are larger, so there are even fewer of them) the effect is not quite as clear-cut as that, but the trend is definitely downward (we need someone with math skills to
design a mathematical model for this).
[note: I don't think today that the LDL-C receptor will be upregulated so much, if at all, if the diet is high in cholesterol and restricted in PUFA]
Further, on a high-fat diet there is also a very significant drop in
pro-inflammatory cytokines involved in liver fibrosis and autoimmunity
(which are connected to and driven by insulin) - see Volek et.al.
There are other benefits too: the food being nutrient dense puts less
work on the gut, and extracting energy from fats requires fewer
vitamins and minerals compared to carbohydrate metabolism. Oxidising a
long-chain saturated fat to ATP involves the same reaction over and
over, which is economical, whereas oxidising glucose involves a
different reaction at each step. This is why refined carbohydrates and
foods high in sugar and starch cause vitamin and mineral deficiencies,
while meat contains all the nutrients needed to process the fats it
contains.
Further, diets high in highly saturated fats such as coconut oil, palm oil, and beef tallow are able to reverse liver fibrosis (Mezey, also Nanji et.al.), while high-PUFA vegetable oils promote liver damage in inflammatory conditions. DHA and lecithin are exceptions to this rule.
The ideal diet for Hep C, according to this hypothesis (and borne out by my experience over the past year) is a diet rich in animal protein and animal fat, with some fish but mostly red meat and eggs, in which most carbs come from green, leafy vegetables. Coconut and coconut cream are used with fish, and grains are completely avoided, as are all sugars except dark honey, fruit juice except small amounts of pomegranate, legumes are restricted to small infrequent servings, all potato is replaced with small servings of sweet potato and pumpkin. Food that needs fat is cooked in beef tallow or butter. Cold pressed virgin olive oil and sm all amounts of sesame seed oil are the only liquid oils used. Nuts and seeds are eaten occasionally. Berries are the main fruit, with small amounts of apple, mango, and apricot [I have no idea now why these particular fruits were my exceptions to the no-fructose rule. Today I'd prefer citrus, and the occasional banana]. Spices are used often; cheese and yoghurt are preffered to milk and milk solids.
As for the objection that this diet may elevate cholesterol, high cholesterol levels in Hep C are associated with less fibrosis and a better response to interferon-ribavirin. This is a diet that elevates HDL-c and lowers triglycerides, which are better proxy markers than cholesterol alone.
Antioxidant supplements including Co-Q10, selenium, tocopherols, zinc, ascorbate, grape seed extract, plus krill oil or cod liver oil and vitamin D3 are taken.
Also, supplements supplying 400mg calcium and 150mg magnesium are taken with each meal of meat or high-iron vegetables to significantly reduce iron uptake.
Glucosamine and niacinamide, plus B12 and folate are used to promote normal iron metabolism and erythropoesis if necessary.
This hypothesis first published (c) 2010 by George D. Henderson, Huia, Auckland, New Zealand
While looking for this, I also found the Atkins website recommendations for Hepatitis. These are pretty much the supplements I used to take, some of which I still use.
FYI, here is my current supplement regime:
100mg co-enzyme Q10
120mg Enzogenol pine bark extract (or 200mg grape seed extract)
4mg astaxanthin
Lactobaccilus rhamnosus and bifidus probiotic
Magnesium (as CMD) with salt
Vitamin D (10,000 iu 2x weekly)
Vitamin K2 (MK7) 90mcg daily
vitamin E 130iu (in above supps, or I probably wouldn't bother)
vitamin C 60mg (ditto, but I'd take 500mg 2x daily if I had it)
I also eat some brazil nuts every day for extra selenium, and eat liver regularly for retinol, copper, etc.
What do I do in my spare time? This.
Thanks for reading this blog so patiently and critically, now it's time to relax and enjoy a song: "Secret Holiday" by The Puddle. http://thepuddle.bandcamp.com/releases
![]()
It was posted on the Life Extension Foundation forum on 27 Feb 2011.
I started restricting carbs after reading "Protein Power" by Michael and Mary Eades, where the rationale for reducing inflammation by restricting carbs and eating more fats is spelled out.
This was good, but it wasn't till I read "Dr Atkin's New Diet Revolution" that I saw the link between what happens to VLDL/TG on ketogenic diets, and what HCV does to exploit lipids.
Next, I found out about the Nanji-French research that demostrates a liver-protective role for saturated fat, and tried limiting PUFA.
Then (about October 2010) I started to get the results I wanted and was ready to write about it, so I posted about it on MySpace (remember MySpace? Tom you bastard, I want my customized settings back!) then posted this at LEF (to date there have been no responses).
http://ask.lef.org/1620/Atkins-Paleo-Diet-for-treatment-of-Hepatitis-C?keywords=DIET&pageindex=1
the HCV virus
is linked exclusively to lipid metabolism (blood fats, commonly but
erroneously called "cholesterol").
- HCV virion is completed by enzyme DGAT, which also packages fats
(triglycerides) prepared by the liver.
- HCV virion escapes infected liver cells via VLDL-c expression.
VLDL-c (very low density lipoprotein cholesterol) carries fats made by
the liver to cells that need them, also carries cholesterol and
lecithins made by the liver.
- HCV virion enters uninfected liver cells via LDL-c receptor. LDL-c
is remains of VLDL-c after fats have been delivered. The fewer
triglycerides, the larger the VLDL-c and LDL-c, hence the fewer interactions there will be with receptors.
This is why HCV only infects the liver - only hepatocytes have all of
these enzymes and receptors.
Now, where do triglycerides and VLDL-c come from? Over half comes from
the carbohydrate in the modern high-carbohydrate diet, converted to
fats for storage or energy, and this half is not produced at all on
high-fat diets.
In other words, on a high-fat, very-low-carb diet, serum levels of
triglycerides (FAT = Fatty Acid Triglycerides) and VLDL-c are
approximately 50% of the levels seen on a low-fat diet.
This diet should automatically reduce the HCV viral load by a similar
amount and the reduction should continue over time. Because the LDL-c
receptor is upregulated on the high-fat diet, probably increasing
uptake of HCV (yet the LDL-c are larger, so there are even fewer of them) the effect is not quite as clear-cut as that, but the trend is definitely downward (we need someone with math skills to
design a mathematical model for this).
[note: I don't think today that the LDL-C receptor will be upregulated so much, if at all, if the diet is high in cholesterol and restricted in PUFA]
Further, on a high-fat diet there is also a very significant drop in
pro-inflammatory cytokines involved in liver fibrosis and autoimmunity
(which are connected to and driven by insulin) - see Volek et.al.
There are other benefits too: the food being nutrient dense puts less
work on the gut, and extracting energy from fats requires fewer
vitamins and minerals compared to carbohydrate metabolism. Oxidising a
long-chain saturated fat to ATP involves the same reaction over and
over, which is economical, whereas oxidising glucose involves a
different reaction at each step. This is why refined carbohydrates and
foods high in sugar and starch cause vitamin and mineral deficiencies,
while meat contains all the nutrients needed to process the fats it
contains.
Further, diets high in highly saturated fats such as coconut oil, palm oil, and beef tallow are able to reverse liver fibrosis (Mezey, also Nanji et.al.), while high-PUFA vegetable oils promote liver damage in inflammatory conditions. DHA and lecithin are exceptions to this rule.
The ideal diet for Hep C, according to this hypothesis (and borne out by my experience over the past year) is a diet rich in animal protein and animal fat, with some fish but mostly red meat and eggs, in which most carbs come from green, leafy vegetables. Coconut and coconut cream are used with fish, and grains are completely avoided, as are all sugars except dark honey, fruit juice except small amounts of pomegranate, legumes are restricted to small infrequent servings, all potato is replaced with small servings of sweet potato and pumpkin. Food that needs fat is cooked in beef tallow or butter. Cold pressed virgin olive oil and sm all amounts of sesame seed oil are the only liquid oils used. Nuts and seeds are eaten occasionally. Berries are the main fruit, with small amounts of apple, mango, and apricot [I have no idea now why these particular fruits were my exceptions to the no-fructose rule. Today I'd prefer citrus, and the occasional banana]. Spices are used often; cheese and yoghurt are preffered to milk and milk solids.
As for the objection that this diet may elevate cholesterol, high cholesterol levels in Hep C are associated with less fibrosis and a better response to interferon-ribavirin. This is a diet that elevates HDL-c and lowers triglycerides, which are better proxy markers than cholesterol alone.
Antioxidant supplements including Co-Q10, selenium, tocopherols, zinc, ascorbate, grape seed extract, plus krill oil or cod liver oil and vitamin D3 are taken.
Also, supplements supplying 400mg calcium and 150mg magnesium are taken with each meal of meat or high-iron vegetables to significantly reduce iron uptake.
Glucosamine and niacinamide, plus B12 and folate are used to promote normal iron metabolism and erythropoesis if necessary.
This hypothesis first published (c) 2010 by George D. Henderson, Huia, Auckland, New Zealand
While looking for this, I also found the Atkins website recommendations for Hepatitis. These are pretty much the supplements I used to take, some of which I still use.
FYI, here is my current supplement regime:
100mg co-enzyme Q10
120mg Enzogenol pine bark extract (or 200mg grape seed extract)
4mg astaxanthin
Lactobaccilus rhamnosus and bifidus probiotic
Magnesium (as CMD) with salt
Vitamin D (10,000 iu 2x weekly)
Vitamin K2 (MK7) 90mcg daily
vitamin E 130iu (in above supps, or I probably wouldn't bother)
vitamin C 60mg (ditto, but I'd take 500mg 2x daily if I had it)
I also eat some brazil nuts every day for extra selenium, and eat liver regularly for retinol, copper, etc.
What do I do in my spare time? This.
Thanks for reading this blog so patiently and critically, now it's time to relax and enjoy a song: "Secret Holiday" by The Puddle. http://thepuddle.bandcamp.com/releases
