Why the High-Fat Hep C Diet? Rationale and n=1 results.

[pinned post hence the unusual date]

I originally started this blog to publicise the hypothesis that a diet low in carbohydrate and linoleic acid, but high in saturated fat and long-chain PUFA, will inhibit HCV replication.

The blog header with the pig above is the abstract for this hypothesis.

I first worked this out in 2010 after reading Dr Atkins New Diet Revolution while studying HCV replication. The lipid patterns in low-carb dieters - low TG and VLDL, high HDL, normal or high LDL - are those associated with lower viral load and improved response to treatment in HCV cases.
The mechanics of HCV replication and infection support this link.

HCV inhibits PPAR-a, a ketogenic diet reverses this inhibition

I wrote a fairly comprehensive version of the hypothesis in 2012:
http://hopefulgeranium.blogspot.co.nz/2012/02/do-high-carbohydrate-diets-and-pufa.html

Recently I was sent a link to an article that cited this paper:
http://www.journal-of-hepatology.eu/article/S0168-8278(11)00492-2/pdfHCV and the hepatic lipid pathway as a potential treatment target. Bassendine MF, Sheridan DA , Felmlee DJ, et al. Journal of Hepatology 2011 vol. 55 j 1428–1440

This review compiles a great deal of supporting evidence regarding the interaction between HCV and lipids, and between lipids and HCV. The only thing missing is the role of carbohydrate. It mentions multiple lipid synthetic pathways as targets for indirect-acting antiviral drugs (IDAA), pathways which are also well documented as targets of low carbohydrate ketogenic diets, or of saturated fat in the diet (in the case of the LDL-receptor complex).

From 2012:
A little n=1 experimental data; 4 years ago (2008) my viral load was 400,000 units, now after 2 years of low carb dieting and intermittent mild ketosis (2012) it is 26,000.

Later in 2012:Total Cholesterol:  6.7  H     
Triglyceride:          0.8         
HDL:                     1.63              (63.57)
LDL (calc.)            4.7   H    
Chol/HDL ratio:     4.1          

HCV viral load on this day (21st May 2012): 60,690 IU/mL (4.78 log)



Lipid panel from 07 Feb 2012, during ketogenic diet phase (non-fasting)

Total Cholesterol: 8.9   HH  (347.1)
Triglyceride:         1.3          (115.7)
HDL:                    1.65         (64.35)
LDL (calc):           6.7    H    (261.3)
Chol/HDL ratio:     5.4   H

HCV viral load on this day: 25,704 IU/mL (4.41 log)

From 2014:
On a personal note, I have started an 8-week trial of Sofosbuvir and GS-5816 (Vulcan). It is day 11 and it seems tolerable so far.
A pre-trial blood test on 22nd October was normal except for these counts:
AST 74
ALT 174
and viral load was 600,419 (log 5.78), counts consistent with the tests I've had done this last year.

But the day the trial started, 18th November, before my first dose, things were different:
AST 21
ALT 32
Viral load 27,167 (log 4.43)

The low viral load is easy to explain; I get a consistent 1 log drop (to 14,000-60,000*) when I try to eat very low carb (50g/day or lower) and an elevation to 400-600,000 when my carbohydrate intake is over 50g/day. When I ate very high carb (but took antioxidant supps) it was as high as it was on 22nd October. So for me the tipping point seems to be where ketosis begins, and other variations don't have much effect; it's an on/off switch, not a dial (and the name of that switch is PPAR-alpha).
[edit: though the very low scores are at ketogenic, or nearly so, carb intakes, the exact increase in carbohydrate needed to cause a significant increase in viral load seemed to vary]
(I do however, according to CAPSCAN elastography, have zero excess fat in my liver, which is an effect of low carb in general, as well as avoiding vegetable seed oils).
My belief is that my viral load was much higher than any of these counts previous to 2003. This was the year I started taking antioxidant supplements, eating a bit better (in a normal, confused "healthy eating" pattern), and using herbal antivirals like silybin. Prior to that I was seriously ill, and I believe that my viral load would have reflected my extra autoimmune symptoms, signs of liver failure, and elevated enzymes. Unfortunately in those days one didn't get a PCR unless one was considering donating one's body to interferon, which I was not.

* I don't seem to have a record of the date of the 14,000 VL reading, but will include it when I find it.

Summary:
A very low carbohydrate ketogenic diet, without enough PUFA to lower LDL artificially, had a significant inhibitory effect on HCV viraemia in my case.
Effective DAA drugs for HCV infection are now available. There is a ~98% SVR rate at present. These drugs are expensive, they sometimes have side effects (though much less so than interferon + ribavirin), and interferon + ribavirin is still being used.
If my results are more generally applicable, VLCKD diet offers an adjunct therapy for patients with a high viral load, steatosis that relates to diet and lifestyle as well as HCV infection, or a need to postpone treatment. In people who oppose or cannot complete or afford treatment, it offers a way to manage the disease, and in particular to reverse the autoimmune syndromes caused by immune complexes when viraemia is excessive.

Two important new papers on climate change.

Whad'ya mean, this has to last me a year?

People in the LCHF community can be resistant to considering climate change and greenhouse gas levels because this argument can be used to shift the goalposts in a clumsy, overt fashion in order to sidestep the evidence on health and keep everyone eating nutrient-poor diets.
Our critics even use these manufactured opportunities to resuscitate their zombie saturated fat and TMAO hypotheses, knowing that most of the audience for ecological debates has no clue how intellectually bankrupt and scientifically desperate these arguments are and have been for some time.
So people can be forgiven for both hiding their heads in the sand and distrusting all "consensus" authority - in our specific area of health, consensus authority has been damagingly wrong for many people's entire lifetimes. And ironically some of this wrongness, the saturated fat question, has contributed to global warming - we'll discuss how later.

However, I for one believe in keeping a close eye on existential threats, and whether you see climate change as a threat to your access to a diet that will keep you healthy, or merely as a threat to the future of human existence on this planet, I think you should too.
Don't listen to headlines, certainly don't listen to the dodgy and ideologically skewed EAT-Lancet commision, but do listen out for the people doing the hard work; the people working out how we should most accurately measure the things that the usual suspects want us to think were measured most accurately back when the results were more favourable to them.
And try to understand the systems involved.

There are essentially two - the usual cycling of carbon through plants and animals back into the atmosphere, which has shaped our climate through most of our history, with fluctuations due to  deforestation and reforestation that mattered (as we shall see) yet did not wipe out life on Earth.
And then there is the geological cycle - carbon from Earth's hothouse youth slowly trapped under the crust as fossil hydrocarbons, which make excellent fuel.
The system of free trade and free travel that fossil fuels allow has replaced warfare since WW2 for most of the world's countries; but it is a potlatch peace, dependent on wasteful gestures, firstly the making and transportation of shit that will either be thrown away, or that in most cases could be made closer to home with lower energy costs, in order to keep wages at a level consistent with a desire for peace, and secondly the transportation of people who will stay in herds or on their phones at the world's beauty spots, only visited for the bragging rights, and for something to do instead of making war against the people who live there.

In the ecological cycle, plants sequester CO2 as they grow, though the soil around them, if very fertile, will release methane (CH4) - recently noted with alarm in the Amazon rainforest, as well as in rice paddies.
CO2 in plants is released by forest or grass fires, and by the metabolism of animals that eat them, which also sequester some of the carbon in their bodies during their lives, mainly in stored fat and protein. When plants and animals rot to return nutrients to the soil this can also release methane, as can the fermentation of plants in the gut by bacteria - the bacteria in the foregut of ruminants are great at processing inedible (to us) fibre to energy substrates, so are high producers of methane (which escapes in burps, not farts).

Our first paper looks at the contribution of methane to the warming effect. CH4 is much more warming than CO2. This is why we hear that 51% of NZ's GHG come from agriculture, when the proportionate amount of CH4 released by ruminants compared to fossil fuel CO2 in NZ each year is much smaller than this - because GHG emissions have, till now, been calculated on the warming effect of each gas. However CO2 lasts for hundreds of years; CH4 has a half-life of only 10 years before turning to CO2. Thus, if we are looking at a 10-year GHG emissions target, half the CH4 should be counted as CO2, and the further out we get, the smaller the difference between CH4 and CO2 gets.
The full model is more complex than this, but the gist of it is the mathematical demonstration that GHG as methane is being badly overestimated whenever the calculation is for a long term impact.

Climate mitigation: An improved emission metric 

A new approach allows the temperature forcing of CO2 and short-lived climate pollutants (SLCPs) to be examined under a common cumulative framework. While anthropogenic warming is largely determined by cumulative emissions of CO2, SLCPs—including soot, other aerosols and methane—also play a role. Quantifying their impact on global temperature is, however, distorted by existing methodologies using conventional Global Warming Potentials (GWP) to convert SLCPs to "CO2-equivalent" emissions. A team of international scientists led by Myles Allen at the University of Oxford provide a solution. A modified form of GWP—GWP*, which relates cumulative CO2 emissions with contemporary SLCP emissions—is shown to better represent the future climate forcing of both long- and short-term pollutants. Use of GWP* could improve climate policy design, benefiting mitigation strategies to achieve the Paris Agreement targets.

Dr Michelle Cain explains the meaning of this paper in this twitter thread and this short YouTube video.

You can't get fossil fuels off the hook. The billionaire owners of EAT-Lancet make their money from a hotel chain. No doubt the hotels are eco-friendly and serve vegan meals. But you can't fill hotels without jet aircraft and cars and cruise ships. Without unnecessary travel, that is - because people with sounder reasons to travel tend to stay with family or friends. A successful hotel chain today is a prime symptom of the fossil fuel binge-for-gold mentality that is breaking the planet.



Our second paper looks at the effects of reforestation on the climate after 56 million mesolithic farming peoples died following the colonisation of the New World.[2] It supplies the evidence for an earlier claim that when their disused cropland was overtaken by forest regrowth, the additional retention of CO2 carbon involved in the creation of standing forests caused the Little Ice Age. Animal numbers are not mentioned in the paper but it is extremely unlikely that ruminant numbers in the Americas declined as a result of the tragic deaths, mainly through introduced diseases, of much of the human population that hunted them. Any additional methane release during forest regrowth also did not stop the Ice Age.



Again, this paper revises the estimates used in GHG calculations - the retention of carbon in forests was missed before - again a case of early GHG formulas missing the all-important effect of time scaling.

Now, let's do some modelling of our own. It's silly, I admit, but no sillier than anything EAT-Lancet have proposed. We have an obesity epidemic; a 2012 estimate of the extra food needed to maintain that extra weight was, that biomass due to obesity was 3.5 million tonnes, the equivalent of 56 million people of average body mass (1.2% of human biomass globally).[3] In other words, if the obesity epidemic could be entirely reversed, the food savings would be roughly equivalent to the annual food consumption of Australia and Canada combined (minus that of little New Zealand).
The reduction in biomass would also be exactly the same as the population drop that caused the Little Ice Age.

In our model all the weight lost is lost because of a reduction in wheat, corn, rice and sugar consumption, and their cropland is replaced by permanent forest (not forestry). Of course farming today is more intensive, and thus causes more harm to biodiversity, soil health, and marine health, so the total hectarage saved will be less - but we can compensate for that if we also tell people they can eat the fat from the animals they eat instead of soy oil or palm oil. This will reduce demand for the two human foods that most drive deforestation. If palm and soy plantations collapse as a result and the Indonesian and Brazilian rainforest takes back the land, so much the better.
Of course, the Adam Curtis voiceover should be telling you about now, "but it was a fantasy". But it was a fantasy that demonstrates how misguided public health experts and their inability to correct error on the saturated fat question have helped to change the climate. We can afford to eat meat, we just can't afford to keep eating lean meat and avoiding the fat-and-cholesterol rich parts of the animal. We can't afford to keep cooking exclusively with vegetable oil (and then often throwing it away). Keep on crowbarring that rubbish advice into climate change statements and no-one but vegans will ever believe you.

References

[1] Myles R. Allen, Keith P. Shine, Jan S. Fuglestvedt, Richard J. Millar, Michelle Cain, David J. Frame & Adrian H. Macey. A solution to the misrepresentations of CO2-equivalent emissions of short-lived climate pollutants under ambitious mitigation. NPJ Climate and Atmospheric Science volume 1, Article number: 16 (2018).

[2] Alexander Kocha, Chris Brierley, Mark M.Maslina, Simon L.Lewis. Earth system impacts of the European arrival and Great Dying in the Americas after 1492. Quaternary Science Reviews
Volume 207, 1 March 2019, Pages 13-36. https://doi.org/10.1016/j.quascirev.2018.12.004

[3] Walpole SC, Prieto-Merino D, Edwards P, Cleland J, Stevens G, Roberts I. The weight of nations: an estimation of adult human biomass. BMC Public Health. 2012;12:439. Published 2012 Jun 18. doi:10.1186/1471-2458-12-439 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3408371/