To kick things off, what is foie gras?
It can be explained with a short missive from our friend Wikipedia:
The California foie gras law, California S.B. 1520, is a California State statute that prohibits the “force feed[ing of] a bird for the purpose of enlarging the bird’s liver beyond normal size”…
Former Senator John Burton called foie gras production “an inhumane process that other countries have sensibly banned.”
Given this outrage related to mistreating birds, you might be surprised to learn that human foie gras industries are booming. Children’s livers are apparently particularly tasty. Not unlike veal, I suppose.
I’m putting $50K of my own money into related investments, but we’ll get back to that in a minute. First, some background…
For most of the 20th century, fatty liver and liver cirrhosis had two primary causes: drinking too much alcohol (e.g. Mickey Mantle) or hepatitis B or C (via IV drug use, unhygienic tattooing, tainted blood transfusions, etc.).
But in the last few decades, even infants are showing up with livers that should belong to hardcore alcoholics. And the numbers aren’t small.
It’s estimated that one in ten American children now suffer from non-alcoholic fatty liver disease (NAFLD), alongside 40 million affected adults. If you’re an obese Mexican-American boy, the odds are 50-50 (!) that you have NAFLD, thanks to genetic predisposition (PNPLA3 gene).
15 years ago, this disease was unheard of. In 10 years, it’s projected to be the #1 cause of liver transplants. Put another way — In 2001, NAFLD was the reason for 1 out of every 100 liver transplants; by 2010, it was up a ten-fold to 1 in 10; by 2025, assuming nothing stems this tide, there could be five million Americans who need new livers because of it.
Who are driving this trend?
Some point fingers at good folks such as Coca-Cola, juice “cocktail” manufacturers, and the like. Given that many researchers blame fructose, it’s not a huge stretch. Personally, the whole thing makes me sick. I’d like to sic the best scientists in the country on them.
Ah, and this is where the good news comes in.
There is a way, albeit an indirect way, to do this. I implore you to read on and bear with me. This is where it gets exciting.
The NIH alone has spent $155 billion on cancer research since 1972, and cancer survival is up a paltry 3% as a result. The US government spends over $25 billion EACH year on HIV/AIDS. That’s a lot of money.
One might assume fatty liver disease would require similar sums. After all, more American adults have NAFLD than prostate cancer, Alzheimer’s disease, heart disease, or type 2 diabetes.
That’s the disconnect…and the opportunity to be part of history.
Enter the “Manhattan Project of Nutrition”
The Nutrition Science Initiative–NuSI–has been called the “Manhattan Project of nutrition.” They are run like a lean startup, and I’m proud to be a part of their advisory board.
They don’t take industry money, so they have no interests to protect.
They believe the NAFLD epidemic can be curtailed for a total of $50 million, but the whole domino effect starts with just $1 million. It is a rare day in science when fundamental questions about an epidemic can be answered with such little money (respectively). It’s an incredible Archimedes lever.
For context, NuSI argues that there are dietary triggers of diseases, including obesity, type 2 diabetes, cancer, and fatty liver disease. To determine what the triggers are, NuSI assembles teams of the best scientists in the country (e.g., from Stanford, Harvard, Columbia, NIH, UCSF, UCSD, Emory, etc.) to fund and execute the kind of research nobody else is willing (or able) to perform.
For NAFLD, NuSI’s team of experts have designed three trials to determine the respective roles of too many calories, too many carbohydrates, and too much sugar–the leading three hypotheses–as dietary triggers.
In early 2015, this team will begin the first ever controlled clinical trial to see if removing sugars from the diet can reverse fatty liver disease in children.
40 kids with NAFLD will be split into two groups, with 20 simply observed on their normal diet as controls, and 20 provided with a diet that’s identical to what they usually eat, but completely devoid of added or refined sugars. The scientists’ hypothesis is that the sugar-free diet will at least stop the progression of NAFLD in these kids, and may even reduce the amount of fat in their livers.
If that’s the case, it’ll be the best evidence we have linking sugar to fatty liver disease.
My $50,000 Challenge…And How to Get Involved
I’m personally matching up to $50,000 for whatever is raised through this blog post, and every donation–big or small–makes a major difference.
[UPDATE: An anonymous donor — a generous reader of this blog — has offered to match up to another $150,000. That means that if you all help donate or contribute just $200,000, another $200,000 will be matched for a total of $400,000!]
Any donation is also a tax write-off, as NuSI is a non-profit organization (of course, speak with your tax advisor). Perfect for end-of-the-year giving.
NuSI is looking to raise $1 million dollars for the first of these three trials—the one that determines how the rest get done. The snowball that starts the avalanche. There are few chances in the world to have this type of impact for this type of money. Could it end up forcing labeling changes, product modifications, obligatory package warnings, policy shifts, and more? I believe so.
Supporting this campaign very easy, and remember–I’m excited to be putting my own skin in this game. I sincerely hope you join me. Every bit counts.
There are three options:
1. Donate by credit or debit card. Visit: http://nusi.org/donate. Enter your donation amount, indicate “NAFLD — Tim Ferriss” in the message field, and click “Donate.” Done.
2. Donate by check. Send your check to: NuSI, attention: Lacey Stenson, 6020 Cornerstone Court W. Suite 240, San Diego, CA 92121. Be sure to write “NAFLD – Tim Ferriss” in the memo line.
3. Donate by transferring securities (stocks, etc.). Email TimFerriss1million@nusi.org [remember the double “r” and double “s”] and they’ll do as much heavy lifting as possible.
Thank you for reading, and thank you for supporting if you’re able. This is a good fight.
If you’d also like to hear a fascinating chat with Peter Attia, MD, co-founder of NuSI, I interview him here on radical sports experimentation, synthetic ketones, meditation, and more. He’s a competitive ultra-endurance athlete, MD, surgeon, and obsessive self-tracker, so we get along great :)
Relevant reading and citations:
Browning JD et al. Prevalence of hepatic steatosis in an urban population in the United States: Impact of ethnicity. Hepatology, 2004.
Welsh JA, Karpen S, Vos MB. Increasing prevalence of nonalcoholic fatty liver disease among United States adolescents, 1988-1994 to 2007-2010. Journal of Pediatrics, 2013.
Targher G, Day CP, Bonora E. Risk of cardiovascular disease in patients with nonalcoholic fatty liver disease. The New England Journal of Medicine, 2010.
Dudekula A et al. Weight loss in nonalcoholic fatty liver disease patients in an ambulatory care setting is largely unsuccessful but correlates with frequency of clinic visits. PLoS One, 2014.
Kawasaki T et al. Rats fed fructose-enriched diets have characteristics of nonalcoholic hepatic steatosis. The Journal of Nutrition, 2009.
Sanchez-Lozada LG et al. Comparison of free fructose and glucose to sucrose in the ability to cause fatty liver. European Journal of Nutrition, 2010.
Best CH et al. Liver damage produced by feeding alcohol or sugar and its prevention by choline. British Medical Journal, 1949.
Ouyang X et al. Fructose consumption as a risk factor for non-alcoholic fatty liver disease. Journal of Hepatology, 2008.
Abid A et al. Soft drink consumption is associated with fatty liver disease independent of metabolic syndrome. Journal of Hepatology, 2009.
Abdelmalek MF et al. Increased fructose consumption is associated with fibrosis severity in patients with nonalcoholic fatty liver disease. Hepatology, 2010.
Assy N et al. Soft drink consumption linked with fatty liver in the absence of traditional risk factors. Canadian Journal of Gastroenterology, 2008.
Stanhope KL et al. Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans. The Journal of Clinical Investigation, 2009.
Maersk M et al. Sucrose-sweetened beverages increase fat storage in liver, muscle, and visceral fat depot: a 6-mo randomized intervention study. The American Journal of Clinical Nutrition, 2012.
Browning JD et al. Short-term weight loss and hepatic triglyceride reduction: Evidence of a metabolic advantage with dietary carbohydrate restriction. American Journal of Clinical Nutrition, 2011.
Vos MB, Lavine JE. Dietary fructose in nonalcoholic fatty liver disease. Hepatology, 2013.
Chung M et al. Fructose, high-fructose corn syrup, sucrose, and nonalcoholic fatty liver disease or indexes of liver health: a systematic review and meta-analysis. The American Journal of Clinical Nutrition, 2014.