Is There and Optimal Diet For Liver Fat (Hepatic Steatosis)?

Stages of liver damage: Healthy, fatty liver, fibrosis, and cirrhosis

From Dr Bret Scher at DietDoctor:

Fortunately, we have emerging evidence that low-carb and ketogenic diets improve fatty liver while also helping with glycemic control and weight loss, an impressive combination rarely seen with medications. As we reported earlier, studies have shown that carbohydrate restriction changes liver metabolism, stimulating the breakdown of liver fat. Another study mentioned in the same post showed that when children substitute sugar for more complex forms of starch, they experience reduced amounts of liver fat.

Yet another impressive study found that despite equal weight loss, a low-carb Mediterranean diet was better than a low-fat diet for reversing liver fat and signs of NAFLD. And finally, Virta Health published a subset of its data showing that one year on a ketogenic diet improved non-invasive tests for NAFLD and liver scarring.

Source: Limiting Carbs Likely Better Than Drugs for Fatty Liver — Diet Doctor

Steve Parker, M.D.

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U.S. Life Expectancy Decreasing

Sir John Glubb studied various empires that existed over the last 4,000 years. He deduced that empires have predictable lifecycles, from origin to ascendence, to great power then decline and collapse. I’m not the only one to notice that the U.S. may be on the decline. Decreasing life expectancies are a potential marker of decline. Glubb died in 1986 at the age of 88.

From JAMA Network:

U.S. life expectancy increased for most of the past 60 years, but the rate of increase slowed over time and life expectancy decreased after 2014. A major contributor has been an increase in mortality from specific causes (eg, drug overdoses, suicides, organ system diseases) among young and middle-aged adults of all racial groups, with an onset as early as the 1990s and with the largest relative increases occurring in the Ohio Valley and New England. The implications for public health and the economy are substantial, making it vital to understand the underlying causes.

Source: Life Expectancy and Mortality Rates in the United States, 1959-2017 | Population Health | JAMA | JAMA Network

Steve Parker, M.D.

PS: Maybe we’d live longer if we ate food congruent with our evolution instead ultra-processed man-made foods.

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Merry Christmas, Everyone!

Credit: Zvonimir Atletic /

Ultra-processed Food Linked to Type 2 Diabetes


One example of UPF

A recent observational study done in France found an association between incidence of type 2 diabetes and consumption of ultra-processed foods.

What are ultra-processed foods? From the study at hand, “Ultraprocessed foods (UPF) (ie, foods undergoing multiple physical, biological, and/or chemical processes, among which mostly of exclusive industrial use, and generally containing food additives) are widespread worldwide and especially in Western diets, representing between 25% and 60% of total daily energy [calories].”

These results suggest an association between UPF consumption and type 2 diabetes risk. They need to be confirmed in large prospective cohorts in other settings, and underlying mechanisms need to be explored in ad hoc epidemiological and experimental studies. Beyond nutritional factors, nonnutritional dimensions of the diet may play a role in these associations, such as some additives, neoformed contaminants, and contact materials. Even if a causal link between UPF and chronic diseases cannot be established so far, the accumulation of consistent data leads public health authorities in several countries such as France or Brazil to recommend privileging the consumption of unprocessed/minimally processed foods, and limiting the consumption of UPF in the name of the precautionary principle.

Source: Ultraprocessed Food Consumption and Risk of Type 2 Diabetes Among Participants of the NutriNet-Santé Prospective Cohort | Lifestyle Behaviors | JAMA Internal Medicine | JAMA Network

Steve Parker, M.D.

PS: Not much UPF in the Paleobetic Diet.

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How to Cure Patello-Femoral Pain Syndrome

Paul Ingraham cured my PFPS. He’s not a physician or physical therapist. But he’s a smart guy, writer, and former massage therapist. I don’t care about your credentials as long as you can help me with your intelligence, integrity, and the scientific method.  Click for his article on patello-femoral pain syndrome if interested. I paid about $20 USD for the full article, and it was well worth it. Full disclosure: I don’t know Paul and earn no commission or other compensation for this endorsement.

Photo credit: Steven Paul Parker II

The key to my cure was probably radical rest, or what Paul calls profound rest.

If you have PFPS, I hope you find something useful here.

Regular readers here know I’m a huge proponent of exercise. Unfortunately, exercise can be risky. You can injure yourself. I did that a few years ago when I was getting in shape to climb Humphreys Peak. I accelerated my training program too rapidly and developed patell0-femoral pain syndrome (PFPS).

This is how my right knee felt in 2017:

I’ve developed over the last month some bothersome pain in my right knee. It’s not interfered much with my actual hiking, but I pay for it over the subsequent day or two. I’m starting to think this may put the kibosh on my Humphries Peak trek next month.

The pain is mostly anterior (front part of the knee) and is most noticeable after I’ve been sitting for a while with the bent knee, then get up to walk. The pain improves greatly after walking for a minute or less. It also hurts a bit when I step up on something using my right leg. If I sit with my knee straight (in full extension), it doesn’t hurt when I get up. The joint is neither unusually warm nor swollen. Ibuprofen doesn’t seem to help it.

That episode resolved after I stopped hiking for 3–4 months. But in 2018 I had recurrence of similar pains in my left knee, with no clear precipitant this time. I continued my usual weight-training program and expected another spontaneous resolution. Six months passed…no improvement. That’s when I found Paul Ingraham’s article.

By the way, I’m the one who diagnosed my PFPS. It’s been said that a doctor who diagnoses and treats himself has a fool for a patient. He can’t be adequately objective.

Alternative diagnoses would include patello-femoral osteoarthritis and degenerative meniscus, due to my age (over 60). Diagnosis of the osteoarthritis could be facilitated by knee X-rays: weight-bearing posterior-anterior imaging, weight-bearing lateral view, and sunrise view.

This was my treatment plan for PFPS in early Feb 2019, based on Paul Ingraham’s recommendations. Paul explains how to do various specific exercises below in his article.

  1. Avoid all activities that stress the patella-femoral joint or aggravate pain for at least two weeks, if not longer (2–3 months). Paul calls it “profound rest.” I started this Feb 17. No knee-loading exercise (e.g., leg presses, any kind of squat, deep knee bends) until pain is truly in remission from rest. I quit my usual squats, Bulgarian split-squats, and single-leg Romanian deadlifts.
  2. Consider Motrin (ibuprofen) 400-600 mg three times daily for two weeks (I did 600 mg 3x/day) but usually no help
  3. Consider cold-packs (10–20 mins) when it flares up but usually no help. (I never did this because I couldn’t find my WalMart cold-pack.)
  4. Find a substitute for the squats? E.g., stationary bike? No bike for now: too much stress on patello-femoral joint at this time
  5. Paul’s not big on stretching (quadriceps and hamstring stretches routinely recommended by others). I didn’t stretch.
  6. While recovering, keep leg straight most of the time, even when sitting. Sit less. (I didn’t sit less but did make a huge effort to keep my  affected led fully extended, or at least not bent more that 20 degrees at any time. This necessitated sitting on the edge of my seat at work, and/or lowering the height of the seat. At home relaxing, I’d keep my leg fully extended. I think this was extremely important for my healing. I considered getting a standing desk for home or work but didn’t.)
  7. Start with exercises that keep knees straight. Exercise both lower extremities. As condition improves, can start to add other exercises, very slowly, that allow bent knees. Single-leg RDLs may be a good start (started in Sept 2019). Restart squats, deep knee bends, and leg presses (cycling?) only very late into recovery. Rehab must progress VERY SLOWLY. If an exercise causes more knee pain, back off and work the hips first. Exercise 2–3 times/week. Walking on the flat in moderation is usually OK. Strengthening hip abductors may be helpful.
  8. Hamstring curls via machine or therabands. Curl to 60 degrees, not 120. (I curled to 90 degrees using therabands).
  9. Quadricep setting. (I didn’t do this. Straight-leg raises on your back seem to be similar, which I did.)
  10. Straight-leg raises, on back and side-lying. (Done: 3 sets of 10 reps each side.)
  11. Clam shells. (Done: 3 sets of 10 reps each side.)
  12. Knee lifts? (don’t know what that is; not done).
  13. Consider the following although not from Paul: Hip abductor strengthening: “monster walks” (lateral steps with elastic band around (just proximal to) knees: 1 min x 3 sets. Hip hikes (what’s this?): 2 sets of 20 reps each side.
  14. Consider the following although not from Paul: Quad strengthening: terminal knee extensions with elastic band, 3 sets of 15 reps; leg presses?; semi squat, 3 sets of 10 reps (also recumbent bike?). Also consider stork stance TKE (terminal knee extensions) as alternative to standard TKE.
  15. Paul likes trekking poles for hikers. (I’ve been using these for years; Leki brand.)
  16. Not from Paul: Home physical therapy for six weeks
  17. Not from Paul: Turkish get-ups now or later? Much further into recovery!

Update of Progress on April 4, 2019:

Knee definitely feeling better, probably due to profound rest as above.  On Feb 23, I aggravated knee mildly by sledding in snow with Paul in Care Free – no regrets! Around Feb 26, Sunny got me started on Platinum’s Ortho-Chon Plus, 3 caps twice daily. Per 3 caps: glucosamine sulfate 800 mg, turmeric 380 mg, methylsulfonylmethane 350 mg, berberine HCL 145 mg, Boswellia serrata extract 140 mg, hyaluronic acid 50 mg, cat’s claw 10 mg, total cetylated fatty acids 3 mg. Not sure if these did any good at all; I’m skeptical. Started feeling less pain around Feb 29.

I am not healed or in remission yet. Doing hip exercises twice or once/wk with Therabands: clamshells, straight leg raises, side-lying straight leg raises, hamstring curls.

I had to put hip exercises on hold temporarily on March 28 due to a right low back muscle strain either from the exercises or weed pulling.

Update on Nov 25, 2019:

The PFPS is in remission and has been since July or so. For the last couple months I’ve been doing single-leg Romanian deadlifts and “walking” on elliptical-type aerobic machines at Anytime Fitness—some machines also work the upper limbs, others don’t—which are very easy on my knees. Avoiding treadmill since I have a palpable click in one knee, and treadmill aggravates my degenerative joint disease (DJD in both knees but predominantly left knee).

Both offending knees

Next step is to slowly re-introduce exercises that load the knees (particularly the patell0-femoral joint). This is scary but must be done. My quads have atrophied somewhat. Squats? Lunges? Bulgarian split squats?

Steve Parker, M.D.

PS: Most types of knee pain will improve if you lose excess fat weight.

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1 in 4 Young Adults in U.S. Has Prediabetes

I’m worried about the kid’s future health

Stats from JAMA Pediatics:

In the United States, about 1 of 5 adolescents [12-18 y.o.] and 1 of 4 young adults [19-34 y.o.] have prediabetes. The adjusted prevalence of prediabetes is higher in male individuals and in people with obesity. Adolescents and young adults with prediabetes also present an unfavorable cardiometabolic risk profile, putting them both at increased risk of type 2 diabetes and cardiovascular diseases.

Source: Prevalence of Prediabetes Among Adolescents and Young Adults in the United States, 2005-2016. – PubMed – NCBI

I’m doing my part to prevent conversion of prediabetes to type 2 diabetes.

Steve Parker, M.D.

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Roll the Dice: Bariatric Surgery Prolongs Life in Type 2 Diabetes

bariatric surgery, Steve Parker MD

Band-type gastric bypass, a type of metabolic surgery

Bariatric surgeries are considered by some experts (mostly surgeons?) to be the most effective way to treat or cure type 2 diabetes. They are effective, assuming you survive the original operation and potential complications, which may require further surgery.

From JAMA Network:

Among patients with type 2 diabetes and obesity, metabolic surgery, compared with nonsurgical management, was associated with a significantly lower risk of incident [heart attack, ischemic stroke, and mortality]. The findings from this observational study must be confirmed in randomized clinical trials.

Source: Association of Metabolic Surgery With Major Adverse Cardiovascular Outcomes in Patients With Type 2 Diabetes and Obesity | Bariatric Surgery | JAMA | JAMA Network

Steve Parker, M.D.

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Can You Avoid Muscle Loss on Low-Calorie Diets?

Greek salad with canned salmon

The parts of your body that aren’t fat tissue are collectively called fat-free mass or lean mass. Fat-free mass includes muscle, organs, bones, water, connective tissue, etc. Reduced-calorie diets are often linked to reduction of body components—like muscle—other than the desired loss of excess fat.

One proven effective way to preserve muscle mass on a reduced-calorie diet is to consume adequate protein. Judicious exercise also helps.

I haven’t read the full article below, and probably won’t. For what it’s worth, the authors say fat-free mass can be preserved during a very low-carb ketogenic diet via adequate intake of vitamin D, leucine, and whey protein. Do you think maybe they’re selling a particular supplement?

The abstract isn’t very well written. Or is it the title that’s misleading?


The loss of fat free mass (FFM) that occurs during a weight loss secondary to low-calorie diet can lead to numerous and deleterious consequences. We performed a review in order to evaluate the till-now evidence regarding the optimum treatment for maintaining FFM during low-calorie diet. This review included eligible studies. In order to maintain FFM during a low-calorie diet, there are various diet strategies: adopt a very-low carbohydrates ketogenic diets (VLCKD) and take an adequate amount of specific nutrients (vitamin D, leucine, whey protein). As regard the numerous and various low-calorie diet proposals for achieving weight loss, the comparison of VLCKD with prudent low-calorie diet demonstrated that FFM was practically unaffected by VLCKD. This is possible for numerous mechanisms, involving insulin and insulin like grow factor-I – growth hormone (IGF-I-GH) axis, and which acts by stimulating protein synthesis. Considering protein and amino acids intake, an adequate daily intake of leucine (4 grams/day), and whey protein (20 grams/day) is recommended.

Regarding vitamin D, if the blood vitamin D has low values (<30 ng/ml), it is mandatory that an adequate supplementation is provided, specifically calcifediol because in the obese subject, this form is recommended to avoid seizure in the adipose tissue: 3–4 drops/day or 20–30 drops/week of calcifediol are generally adequate to restore normal 25(OH)D plasma levels in obese subjects.

Source: Current Opinion On Dietary Advice In Order To Preserve Fat Free Mass During A Low-Calorie Diet – ScienceDirect

I had never heard of that obesity-calcifidiol connection.

Steve Parker, M.D.

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High-Intensity Interval Training (HIIT) Improves Memory in Older Adults, May Prevent Dementia

Steve Parker MD

A slow leisurely pace won’t cut it

Dementia is a devastating and expensive development for an individual and his family. Most dementias are progressive and incurable. If it can be prevented, it should be. Exercise is one preventative. But how much and what kind of exercise?

Nine percent of U.S. adults over 65 have dementia. That’s 3.650,000 folks.

From The Globe and Mail:

In 2017, a team led by the lab’s director, Jennifer Heisz, published a five-year study of more than 1,600 adults older than 65 that concluded that genetics and exercise habits contribute roughly equally to the risk of eventually developing dementia. Only one of those two factors is under your control, so researchers around the world have been striving to pin down exactly what sort of workout routine will best nourish your neurons.

Heisz’s latest study, published last month in the journal Applied Physiology, Nutrition, and Metabolism, offers a tentative answer to this much-debated question. Older adults who sweated through 12 weeks of high-intensity interval training improved their performance on a memory test by 30 per cent compared with those who did a more moderate exercise routine.

This was a small study, only about 20 sedentary participants (all over 60 years old) subjected to one of three protocols for twelve weeks, exercising thrice weekly:

  1. Four-minute bouts of vigorous treadmill walking at 90-95% of maximum heart rate, repeated four times, with three minutes easy walking between the high-intensity spells intervals (HIIT)
  2. Walking at 70-75% of max heart rate for 47 minutes (burning the same number of calories as group #1
  3. Thirty minutes of relaxed stretching

Alex Hutchinson’s full article is well worth a couple minutes of your time if you want to avoid dementia.

Source: New study shows the right workout routine can help fight dementia – The Globe and Mail

Steve Parker, M.D.

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Low-Carb Diets Linked to Premature Death

…and high-carb diets might be just as harmful. In the research at hand, low-carb was defined as under 40% of calories from carbohydrate, and high-carb was over 70% of calories.

Grain-based high-carb Neolithic food

The longevity sweet spot was 50-55% of calories from carbs.

If you want to eat low-carb, read more below to identify the possibly healthier substitutions for carbs. Tl;dr version: Eat plant-derived protein and fats.

From a 2018 study in The Lancet Public Health:


Low carbohydrate diets, which restrict carbohydrate in favour of increased protein or fat intake, or both, are a popular weight-loss strategy. However, the long-term effect of carbohydrate restriction on mortality is controversial and could depend on whether dietary carbohydrate is replaced by plant-based or animal-based fat and protein. We aimed to investigate the association between carbohydrate intake and mortality.


We studied 15 428 adults aged 45–64 years, in four US communities, who completed a dietary questionnaire at enrolment in the Atherosclerosis Risk in Communities (ARIC) study (between 1987 and 1989), and who did not report extreme caloric intake (4200 kcal per day for men and 3600 kcal per day for women). The primary outcome was all-cause mortality. We investigated the association between the percentage of energy from carbohydrate intake and all-cause mortality, accounting for possible non-linear relationships in this cohort. We further examined this association, combining ARIC data with data for carbohydrate intake reported from seven multinational prospective studies in a meta-analysis. Finally, we assessed whether the substitution of animal or plant sources of fat and protein for carbohydrate affected mortality.


During a median follow-up of 25 years there were 6283 deaths in the ARIC cohort, and there were 40 181 deaths across all cohort studies. In the ARIC cohort, after multivariable adjustment, there was a U-shaped association between the percentage of energy consumed from carbohydrate (mean 48·9%, SD 9·4) and mortality: a percentage of 50–55% energy from carbohydrate was associated with the lowest risk of mortality. In the meta-analysis of all cohorts (432 179 participants), both low carbohydrate consumption (70%) conferred greater mortality risk than did moderate intake, which was consistent with a U-shaped association (pooled hazard ratio 1·20, 95% CI 1·09–1·32 for low carbohydrate consumption; 1·23, 1·11–1·36 for high carbohydrate consumption). However, results varied by the source of macronutrients: mortality increased when carbohydrates were exchanged for animal-derived fat or protein (1·18, 1·08–1·29) and mortality decreased when the substitutions were plant-based (0·82, 0·78–0·87).


Both high and low percentages of carbohydrate diets were associated with increased mortality, with minimal risk observed at 50–55% carbohydrate intake. Low carbohydrate dietary patterns favouring animal-derived protein and fat sources, from sources such as lamb, beef, pork, and chicken, were associated with higher mortality, whereas those that favoured plant-derived protein and fat intake, from sources such as vegetables, nuts, peanut butter, and whole-grain breads, were associated with lower mortality, suggesting that the source of food notably modifies the association between carbohydrate intake and mortality.

Source: Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analysis – The Lancet Public Health

Steve Parker, M.D.

PS: This type of research is often unreliable. If you have a better study design or more reliable data, please share with the world.

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