“Thank You” for Your Support!

I published my first book in 2007 to extend my healing reach beyond the confines of the clinic and hospital room. I’m certain my writing has improved the health of many folks I’ll never know about, and that means more to me than any financial success I’ve had with the books.

In 2020, my net profit from writing was $937.08, which is admittedly pitiful. The prior year profit was $5,802.48. Pandemic effect, maybe? To lower my expenses in 2021, I’ll look into a private PO box instead of US Postal Service ($168/year), drop Amazon Prime ($129/year), and negotiate lower fees with Network Solutions.

I am blessed to have a hospitalist job that pays well. COVID-19 has caused major economic hardship for many of you, including unemployment.

My primary means of advertising has been blogging. Cross-posting on Facebook, Twitter, and LinkedIn has done almost nothing for book sales. A few years ago I could give my hospital patients a business card with links to my books, but my employer insisted I stop.

If you care to support my writing, buy a book. If not for yourself, then for someone you care about.

Steve Parker, M.D.

PS: All my books are here and at Smashwords.com.

PPS: Guesstimating my combined federal and state taxes being 40%, I have $562.25 left after paying taxes. And don’t forget sales tax on many things I might buy with that $562.25. 

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Are Insulin Prices Higher Under the Biden Administration?

Roasted Radishes and Brussels Sprouts

Newsweek looks at the issue.

In any case, why not reduce your need for insulin with low-carb eating?

Steve Parker, M.D.

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Non-Alcoholic Fatty Liver Disease: Ketogenic Diet Reduced Liver Fat Quickly

stages of liver damage

There’s a silent epidemic in folks with type 2 diabetes: 50 to 70% have non-alcoholic fatty liver disease. Non-alcoholic fatty liver disease is an important contributor to cirrhosis, i.e., scarring in the liver that impairs liver function. In the study at hand, a ketogenic diet reduced liver fat by 31% over just six days. I don’t have many details of the diet used, but it reduced carbohydrates to 20 grams/day.

Here’s the abstract:

Ketogenic diet is an effective treatment for nonalcoholic fatty liver disease (NAFLD). Here, we present evidence that hepatic mitochondrial fluxes and redox state are markedly altered during ketogenic diet-induced reversal of NAFLD in humans. Ketogenic diet for 6 [days] markedly decreased liver fat content and hepatic insulin resistance. These changes were associated with increased net hydrolysis of liver triglycerides and decreased endogenous glucose production and serum insulin concentrations. Partitioning of fatty acids toward ketogenesis increased, which was associated with increased hepatic mitochondrial redox state and decreased hepatic citrate synthase flux. These data demonstrate heretofore undescribed adaptations underlying the reversal of NAFLD by ketogenic diet and highlight hepatic mitochondrial fluxes and redox state as potential treatment targets in NAFLD.

Weight loss by ketogenic diet (KD) has gained popularity in management of nonalcoholic fatty liver disease (NAFLD). KD rapidly reverses NAFLD and insulin resistance despite increasing circulating nonesterified fatty acids (NEFA), the main substrate for synthesis of intrahepatic triglycerides (IHTG). To explore the underlying mechanism, we quantified hepatic mitochondrial fluxes and their regulators in humans by using positional isotopomer NMR tracer analysis. Ten overweight/obese subjects received stable isotope infusions of: [D7]glucose, [13C4]β-hydroxybutyrate and [3-13C]lactate before and after a 6-d KD. IHTG was determined by proton magnetic resonance spectroscopy (1H-MRS). The KD diet decreased IHTG by 31% in the face of a 3% decrease in body weight and decreased hepatic insulin resistance (−58%) despite an increase in NEFA concentrations (+35%). These changes were attributed to increased net hydrolysis of IHTG and partitioning of the resulting fatty acids toward ketogenesis (+232%) due to reductions in serum insulin concentrations (−53%) and hepatic citrate synthase flux (−38%), respectively. The former was attributed to decreased hepatic insulin resistance and the latter to increased hepatic mitochondrial redox state (+167%) and decreased plasma leptin (−45%) and triiodothyronine (−21%) concentrations. These data demonstrate heretofore undescribed adaptations underlying the reversal of NAFLD by KD: That is, markedly altered hepatic mitochondrial fluxes and redox state to promote ketogenesis rather than synthesis of IHTG.

Source: Effect of a ketogenic diet on hepatic steatosis and hepatic mitochondrial metabolism in nonalcoholic fatty liver disease | PNAS

Steve Parker, M.D.

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Don’t Let Aging Reduce Your Muscle Mass

Exercise is a fountain of youth available to every one

Axel Sigurdsson, MD, PhD, published a great article on prevention of age-related sarcopenia (loss of muscle mass). Click through for details. To stay vigorous as you age, you want to preserve muscle mass and the strength it provides. If you’ve lost muscle mass, you can re-build it. Summary from the good doctor:

Age-related loss of muscle mass (sarcopenia)may start as early as in our thirties and appears to continue for the rest of our lives.

There is also a loss of muscle strength and muscle function. The consequences may often be severe, particularly in the elderly.

Increased physical activity and adequate nutrition are the most powerful tools at our disposal to delay age-related loss of muscle mass.

Well-rounded exercise programs consisting of aerobic and resistance exercises are believed to be most effective

Modification of dietary habits may be an important tool to prevent the decline in muscle mass and function that occurs with aging.

Adequate protein intake is of key importance. Animal-derived protein may provide a higher and broader biological value than vegetable protein.

Fish consumption is recommended and fruits and vegetables should be consumed regularly.

Nutritional supplements containing essential amino acids may be helpful. This is particularly true for whey protein.

Fish-derived protein hydrolysates also appear promising.

Adequate intake of vitamin D is essential.

“Fish-derived protein hydrolysates” doesn’t sound very appetizing. I’ll stick with whole fish for now, especially cold-water fatty fish.

Steve Parker, M.D.

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More Low-Carb Mediterranean Diet Recipes

Ketogenic compatible

Check out Diet Doctor for over 60 low-carb Mediterranean diet recipes! Diet Doctor usually provides carbohydrate counts, so you can fit these into the Low-Carb Mediterranean Diet.

Click on “recipes” at left for my own low-carb Mediterranean diet recipes.

Steve Parker, M.D.

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Advanced Liver Fibrosis Is Common in Patients With Type 2 Diabetes

A 2021 issue of Diabetes Care reveals the shocking prevalence of advanced liver fibrosis (scarring) in folks with type 2 diabetes: one of every six. Fibrosis may eventually lead to cirrhosis and require a liver transplant. The study at hand used vibration-controlled transient elastography to measure liver stiffness. The more fibrosis, the stiffer the liver. The measuring device “uses a pulse-echo ultrasound technique to quantify the speed of mechanically induced shear wave within liver tissue,” which correlates with the severity of fibrosis. Liver fat, i.e., steatosis, can also be quantified at the same time by measuring the ultrasonic attenuation of the echo wave. 

Here’s the study abstract:

OBJECTIVE

Assess the prevalence of nonalcoholic fatty liver disease (NAFLD) and of liver fibrosis associated with nonalcoholic steatohepatitis in unselected patients with type 2 diabetes mellitus (T2DM).

RESEARCH DESIGN AND METHODS

A total of 561 patients with T2DM (age: 60 ± 11 years; BMI: 33.4 ± 6.2 kg/m2; and HbA1c: 7.5 ± 1.8%) attending primary care or endocrinology outpatient clinics and unaware of having NAFLD were recruited. At the visit, volunteers were invited to be screened by elastography for steatosis and fibrosis by controlled attenuation parameter (≥274 dB/m) and liver stiffness measurement (LSM; ≥7.0 kPa), respectively. Secondary causes of liver disease were ruled out. Diagnostic panels for prediction of advanced fibrosis, such as AST-to-platelet ratio index (APRI) and Fibrosis-4 (FIB-4) index, were also measured. A liver biopsy was performed if results were suggestive of fibrosis.

RESULTS

The prevalence of steatosis was 70% and of fibrosis 21% (LSM ≥7.0 kPa). Moderate fibrosis (F2: LSM ≥8.2 kPa) was present in 6% and severe fibrosis or cirrhosis (F3–4: LSM ≥9.7 kPa) in 9%, similar to that estimated by FIB-4 and APRI panels. Noninvasive testing was consistent with liver biopsy results. Elevated AST or ALT ≥40 units/L was present in a minority of patients with steatosis (8% and 13%, respectively) or with liver fibrosis (18% and 28%, respectively). This suggests that AST/ALT alone are insufficient as initial screening. However, performance may be enhanced by imaging (e.g., transient elastography) and plasma diagnostic panels (e.g., FIB-4 and APRI).

CONCLUSIONS

Moderate-to-advanced fibrosis (F2 or higher), an established risk factor for cirrhosis and overall mortality, affects at least one out of six (15%) patients with T2DM. These results support the American Diabetes Association guidelines to screen for clinically significant fibrosis in patients with T2DM with steatosis or elevated ALT.

Source: Advanced Liver Fibrosis Is Common in Patients With Type 2 Diabetes Followed in the Outpatient Setting: The Need for Systematic Screening | Diabetes Care

The good news is that liver fat (aka hepatic steatosis), a precursor to fibrosis, can be reversed to a great degree.

Steve Parker, M.D.

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Gastric Bypass Reduces Diabetic Retinopathy Risk

Photo of the retina at the back of the eyeball

Retinopathy is a fancy word meaning disease of the retina, the light detecting membrane at the back of the eyeball. About two in five folks with diabetes have some form or degree of diabetic retinopathy. The pathology is mostly in the arterial blood vessels of the retina. Keeping blood sugars under good control is one way to prevent diabetic retinopathy. Once diagnosed, it can be treated with injections, lasers, or surgery.

Here’s the abstract from a recent scientific report the looked at the ocular effects of gastric bypass surgery in obese type 2 diabetics. Over the course of 4.5 years, the risk of diabetic retinopathy was 40% less in those who had bypass surgery.

Importance  Knowledge of the incidence and progression of diabetic retinopathy (DR) after gastric bypass surgery (GBP) in patients with obesity and diabetes could guide the management of these patients.

Objective  To investigate the incidence of diabetic ocular complications in patients with type 2 diabetes after GBP compared with the incidence of diabetic ocular complications in a matched cohort of patients with obesity and diabetes who have not undergone GBP.

Design, Setting, and Participants  Data from 2 nationwide registers in Sweden, the Scandinavian Obesity Surgery Registry and the National Diabetes Register, were used for this cohort study. A total of 5321 patients with diabetes from the Scandinavian Obesity Surgery Registry who had undergone GBP from January 1, 2007, to December 31, 2013, were matched with 5321 patients with diabetes from the National Diabetes Register who had not undergone GBP, based on sex, age, body mass index (BMI), and calendar time (2007-2013). Follow-up data were obtained until December 31, 2015. Statistical analysis was performed from October 5, 2018, to September 30, 2019.

Exposure  Gastric bypass surgery.

Main Outcomes and Measures  Incidence of new DR and other diabetic ocular complications.

Results  The study population consisted of 5321 patients who had undergone GBP (3223 women [60.6%]; mean [SD] age, 49.0 [9.5] years) and 5321 matched controls (3395 women [63.8%]; mean [SD] age, 47.1 [11.5] years). Mean (SD) follow-up was 4.5 (1.6) years. The mean (SD) BMI and hemoglobin A1c concentration at baseline were 42.0 (5.7) and 7.6% (1.5%), respectively, in the GBP group and 40.9 (7.3) and 7.5% (1.5%), respectively, in the control group. The mean (SD) duration of diabetes was 6.8 (6.3) years in the GBP group and 6.4 (6.4) years in the control group. The risk for new DR was reduced in the patients who underwent GBP (hazard ratio, 0.62 [95% CI, 0.49-0.78]; P < .001). The dominant risk factors for development of DR at baseline were diabetes duration, hemoglobin A1c concentration, use of insulin, glomerular filtration rate, and BMI.

Conclusions and Relevance  This nationwide matched cohort study suggests that there is a reduced risk of developing new DR associated with GBP, and no evidence of an increased risk of developing DR that threatened sight or required treatment.

Click for full text.

Steve Parker, M.D.

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Mediterranean Diet Linked to Reduced Frailty in the Elderly

Cold-water fatty fish loaded with omega-3 fatty acids include salmon, trout, sardines, herring, and mackerel

In the study at hand, frailty was measured by exhaustion, weakness, physical activity, walking speed, and weight loss. From the Journal of the American Medical Medical Directors Association way back in 2014:

Abstract

Background and objective: Low intake of certain micronutrients and protein has been associated with higher risk of frailty. However, very few studies have assessed the effect of global dietary patterns on frailty. This study examined the association between adherence to the Mediterranean diet (MD) and the risk of frailty in older adults.

Design, setting, and participants: Prospective cohort study with 1815 community-dwelling individuals aged ≥60 years recruited in 2008-2010 in Spain.

Measurements: At baseline, the degree of MD [Mediterranean Diet] adherence was measured with the Mediterranean Diet Adherence Screener (MEDAS) score and the Mediterranean Diet Score, also known as the Trichopoulou index. In 2012, individuals were reassessed to detect incident frailty, defined as having at least 3 of the following criteria: exhaustion, muscle weakness, low physical activity, slow walking speed, and weight loss. The study associations were summarized with odds ratios (OR) and their 95% confidence interval (CI) obtained from logistic regression, with adjustment for the main confounders.

Results: Over a mean follow-up of 3.5 years, 137 persons with incident frailty were identified. Compared with individuals in the lowest tertile of the MEDAS score (lowest MD adherence), the OR (95% CI) of frailty was 0.85 (0.54-1.36) in those in the second tertile, and 0.65 (0.40-1.04; P for trend = .07) in the third tertile. Corresponding figures for the Mediterranean Diet Score were 0.59 (0.37-0.95) and 0.48 (0.30-0.77; P for trend = .002). Being in the highest tertile of MEDAS was associated with reduced risk of slow walking (OR 0.53; 95% CI 0.35-0.79) and of weight loss (OR 0.53; 95% CI 0.36-0.80). Lastly, the risk of frailty was inversely associated with consumption of fish (OR 0.66; 95% CI 0.45-0.97) and fruit (OR 0.59; 95% CI 0.39-0.91).

Conclusions: Among community-dwelling older adults, an increasing adherence to the MD was associated with decreasing risk of frailty.

Did you notice another good reason to eat fish?

I wonder why the research was published in the Journal of the American Medical Medical Directors Association?

Steve Parker, M.D.

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Mediterranean Diet Prevents Cancer in Women But Not Men

Steve Parker MD, low-carb diet, diabetic diet
Olives, olive oil, and vinegar: classic Mediterranean foods

The traditional Mediterranean diet has long been linked to lower risk of certain cancers, particularly colon, breast, uterus, and prostate cancer. That’s one reason the diets usually ranked as the #1 healthiest diet in the U.S. News and World Report’s annual diet survey. A new study of a Netherlands population suggest that the anti-cancer benefit applies only to women. From a 2020 issue of the Journal of the Academy of Nutrition and Dietetics:

In this NLCS analysis, sex-specific associations of a priori defined Mediterranean diet adherence with risks of overall cancer and cancer subgroups defined by relations with 3 major cancer risk factors (tobacco smoking, obesity, and alcohol consumption) were investigated. In women, middle compared with low aMEDr values [alternate Mediterranean diet score without alcohol] were significantly associated with a reduced risk of overall cancer and the majority of the cancer subgroups investigated. Other associations in women were not statistically significant after full adjustment for confounding, but all estimates were below 1. No association was observed between aMEDr and risk of overall cancer or any of the cancer subgroups in men. Inclusion of alcohol in the Mediterranean diet score diminished the model performance.

Even though the association of Mediterranean diet adherence with overall cancer risk is comprised of a combination of potentially diverging associations with individual cancer (sub)types, overall cancer risk is an interesting end point for epidemiological studies. It provides insight in the overall possible benefits of Mediterranean diet adherence and the potential of the Mediterranean diet as a dietary strategy for cancer prevention. Findings of previously conducted prospective studies evaluating the relation between a priori defined Mediterranean diet adherence and overall cancer risk have been inconclusive and were rarely specified by sex.

A priori defined Mediterranean diet adherence has previously significantly been associated with a reduced overall cancer risk in the total European Prospective Investigation into Cancer and Nutrition (EPIC) cohort as well as the Greek EPIC cohort.9,10 Comparing the highest with the lowest Mediterranean diet adherence category in the total EPIC cohort, HRs (95% CIs) of 0.93 (0.88-0.99) and 0.93 (0.89-0.96) were observed for men and women, respectively. Although inverse associations were also suggested for both sexes in the Greek EPIC cohort, only effect estimates obtained in women reached statistical significance (HRhigh vs low [95% CI]: 0.83 [0.63-1.09] for men and 0.73 [0.56-0.96] for women). In addition to the previously mentioned EPIC studies, weak inverse associations between Mediterranean diet adherence and overall cancer risk were observed in men (HRper tertile increase [95% CI]: 0.97 [0.94-1.01]) and women (HRper tertile increase [95% CI]: 0.97 [0.93-1.00]) participating in the Swedish prospective Västerbotten Intervention Programme. In the present analysis of the NLCS cohort, a priori defined Mediterranean diet adherence was not associated with overall cancer risk in men. In regard to women, although the multivariable-adjusted associations in female NLCS participants were not statistically significant in most cases, effect estimates were stronger inverse than those observed for women in the total EPIC cohort, which did reach statistical significance possibly due to the larger number of cases. Additional cohort studies in Germany and France have investigated the association between Mediterranean diet adherence and overall cancer risk in men and women together and did not observe an association. Besides the prospective cohort evidence, a reduced overall cancer risk (borderline significant, P = .05) was indicated in patients with coronary heart disease who followed an α-linolenic acid-rich Mediterranean-type diet as opposed to a control diet close to the step 1 prudent diet of the American Heart Association in the randomized Lyon Diet Heart Study. However, results should be interpreted with caution because they were based on only 24 incident cancer cases.

Source: Adherence to the Mediterranean Diet and Overall Cancer Incidence: The Netherlands Cohort Study – Journal of the Academy of Nutrition and Dietetics

At least we still have unequivocal evidence for the cardiovascular, longevity, and anti-dementia properties of the Mediterranean diet. Or do we?

Steve Parker, M.D.

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Lose Weight With the Mediterranean Diet Despite Pasta

spaghetti squash, spaghetti
Spaghetti squash is an alternative to pasta

The title above sums it up. If you’re eating pasta frequently and trying to lose weight, you do have to be careful not to over-eat. In other words, you generally have to restrict calories. In the study at hand, I don’t know how many daily calories were allowed since I haven’t read the full report. Here’s the abstract:

Background & aims

The effect of pasta consumption within a low-energy [read: calorie-restricted] Mediterranean diet on body weight regulation has been scarcely explored. This paper investigates the effect of two Mediterranean diets, which differed for lower or higher pasta intake, on body weight change in individuals with obesity.

Methods & Results

Forty-nine volunteers finished a quasi-experimental 6-month two–parallel group dietary intervention. Participants were assigned to a low-energy high pasta (HP) or to a low-energy low Pasta (LP) group on the basis of their pasta intake (HP ≥ 5 or LP ≤ 3 times/week). Anthropometrics, blood pressure and heart rate were measured every month. Weight maintenance was checked at month 12. Body composition (bioelectrical impedance analysis, BIA), food intake (24-h recall plus a 7-day carbohydrate record) and the perceived quality of life (36-item short-form health survey, SF-36) were assessed at baseline, 3 and 6 months. Blood samples were collected at baseline and month 6 to assess glucose and lipid metabolism. After 6-month intervention, body weight reduction was −10 ± 8% and −7 ± 4% in HP and LP diet, respectively, and it remained similar at month 12. Both dietary interventions improved anthropometric parameters, body composition, glucose and lipid metabolism, but no significant differences were observed between treatment groups. No differences were observed for blood pressure and heart rate between treatments and among times. HP diet significantly improved perception of quality of life for the physical component.

Conclusions

Independent of pasta consumption frequency, low-energy Mediterranean diets were successful in improving anthropometrics, physiological parameters and dietary habits after a 6-month weight-loss intervention.

Source: Body weight of individuals with obesity decreases after a 6-month high pasta or low pasta Mediterranean diet weight-loss intervention – Nutrition, Metabolism and Cardiovascular Diseases

Steve Parker, M.D.

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