I am so thrilled to have been interviewed by Dr. Danielle Belardo for her Nutrition Rounds Podcast, which has been repeatedly featured in the top ten of all podcasts downloaded on iTunes! If you haven’t checked out her podcast, I highly recommend you do ASAP. She’s interviewed many of the greats (including many of the people that I’ve look up to) in plant-based medicine, including Dr. Dean Ornish, Dr. Joel Kahn (twice!), and Dr. Caldwell Esselstyn, and provides a lot of useful information in each episode.

You can find my interview as Episode 14 here.

Here are the links to many of the studies we discussed:

1. Fast Facts on Kidney Disease
   1. 125,000 new cases of kidney failure each year
   2. 21,000 kidney transplants done each year
   3. 468,000 people on dialysis currently
   4. 5 year survival rate on dialysis is 45%
   5. 3-5 years is the average waiting time to get a deceased donor kidney off the waitlist
2. Information on live and deceased donor kidney donation
3. The UCSF Artificial Kidney Project
4. Overview of how the kidney works
5. Diabetic Kidney Disease
   1. #1 cause of CKD and kidney failure 
   2. A nice review in the Clinical Journal of the American Society of Nephrology on diabetic kidney disease
      1. Evidence of the importance of glucose control in Type 1 Diabetics
         1. DCCT/EDIC
         2. DCCT/EDIC
      2. Evidence of the importance of glucose control in Type 2 Diabetics
         1. UKPDS
         2. UKPDS
   3. How both protein and hyperglycemia cause hyperfiltration in diabetic kidney disease
   4. Papers on Plant-Based Diets to Prevent, Treat, and Reverse Diabetes
      1. Nice review by McMacken et al. 2017 J. Geriatr Cardiol 
6. Hypertensive Kidney Disease
   1. #2 cause of CKD and kidney failure
   2. Secondary analysis of DASH-Sodium trial showing a near 21/8 mm Hg reduction in BP for those with a BP > 150/90 mm Hg
   3. Papers on Plant-Based Diets to Prevent, Treat, and Reverse Hypertension
      1. Nice review by Alexander et al. 
      2. Meta-analysis of vegetarians diets and blood pressure by Yokoyama et al.
7. Listener Questions:
   1. TMAO
      1. Increased TMAO levels are both a product and cause of CKD
   2. Kidney Stones
      1. Evidence that animal protein increases the risk of kidney stones
         1. Borgi study showing a low-protein, low-salt study reduces kidney stone incidence
         2. Another study
         3. “Stone formers should be advised to limit the intake of all animal proteins, including fish.” 
         4. Association of animal protein with kidney stones dating back to WWII
         5. Should recurrent calcium oxalate stone formers become vegetarians?
         6. Fruits and vegetables reduce the risk of kidney stones despite having purines
         7. Potassium citrate, a medication often used to treat kidney stones, has ingredients that are often found in fruits and vegetables
      2. People with documented hyperoxaluria (excess oxalate in the urine determined by a 24 hour urine collection) should consider restricting high-oxalate foods
         1. List of high-oxalate foods
   3. Protein in Chronic Kidney Disease
      1. My paper with Dr. Sanjeev Shah and Dr. Kam Kalantar-Zadeh reviewing the issues of plant protein quantity and quality in CKD
      2. Low-Protein diets in Chronic kidney Disease
         1. Recent review on nutritional considerations in CKD (NEJM review)
            1. Caveat: I disagree with the author’s recommendation for high biologic value protein in CKD. You’ll notice that the same author is a co-author of paper mentioned in the previous point and has since taken on a revised view of plant protein. As we write in that paper, plant-protein is more than adequate in CKD.
         2. Secondary Analyses of MDRD showing a (small, but significant) benefit of low-protein diets
         3. Meta-analysis of low-protein diets on the rate of kidney function decline
   4. What is the evidence that animal protein is harmful for the kidneys for those without chronic kidney disease?
      1. Cross-sectional studies
         1. Nettleton et al. AJCN 2009
         2. Yuzbashian et al. J. of Nephro. 2015
         3. Oosterwijk et al. KI Reports 2019
      2. Prospective observational studies
         1. Haring et al. J Ren N 2017
         2. Lew et al. JASN 2017
         3. Lin et al. CJASN 2010
         4. Lin et al. AJKD 2011
      3. Interventional studies
         1. Kontessis et al. KI 1990 (only study to control for protein QUANTITY – an important confounder in every other study I’ve seen on the subject)
   5. What is the evidence that animal protein is harmful for the kidneys for those with chronic kidney disease?
      1. Observational studies
         1. Knight et al. Annals of IM 2003
      2. Interventional studies
         1. Azadbakht et al. J Ren Nutr 2009
         2. Azadbakht et al. Diabetes Care 2008
         3. Barsotti et al. Nephron 1996
         4. Teixeira et al. J Nutr 2004
   6. What is the best diet for those with CKD?
      1. Although the evidence is generally limited, plant-based diets may be of benefit. Each individual patient is different and monitoring may be required, especially for potassium levels. Here are some recent reviews on the subject of plant-based diets in CKD:
         1. Stewart et al. 2019 JOJ Urology and Nephrology
         2. Chauveau et al. 2018 NDT
         3. Gluba-Brzozka et al. 2017 Nutrients
      2. Plant-based diets have additional (“bonus”) benefits for their ability to treat the following co-morbidities associated with CKD:
         1. Hyperphosphatemia
            1. Moe et al. CJASN 2011
         2. Metabolic Acidosis
            1. Animal protein is acidic
               1. Scialla et al 2013 Adv. Chronic Kidney Dis.
            2. Vegan Diet is nearly acid neutral
               1. Strohle et al. 2011 Ann. Nutr. Metab.
               2. Ausman et al. 2008 J. Ren. Nutr.
            3. Interventional data supporting the use of 2-4 cups of fruits and vegetables for the treatment of metabolic acidosis in CKD. Notice how the fruit and vegetable arms also had lower BPs and weights after the experiment. Also notice the lack of hyperkalemia.
               1. CKD Stages I and II for 30 days
               2. CKD Stage III for 3 years
               3. CKD Stage IV for 1 year
         3. Hypertension
            1. See above section on “Hypertensive Kidney Disease”
         4. Obesity
            1. Turner-McGrievy et al. 2017 J. Geriatr Cardiol
   7. Potassium, Plant-Based Diets, and Kidney Disease
      1. The best (and only) paper on the subject is by St-Jules et al. 2016 J. Ren. Nutr. 
      2. A good editorial on the issue by Moorthi et al. 2019 CJASN
   8. Bellevue’s Plant-Based Lifestyle Clinic

 

Last Updated: April 7, 2019

The keto diet has been widely promulgated as an effective therapy for the treatment of diabetes and weight loss with minimal side effects. The diet may be of benefit for some in select circumstances, but perhaps not for all patients. Many discussions regarding the diet present an unbalanced view, often omitting studies that show harm or lack of a benefit. To balance the narrative, I’ve written this post that I intend to keep maintained for foreseeable future. Below I present the links to references of important studies that are often excluded from the discussion of ketogenic, and by association, low-carbohydrate diets. I invite you to look through them. Personally, I did not expect to find as much as I did (and certainly not so many concerning side effects). If you have other studies or comments, please post them below in the reply section of this page. You can also share them with me on Twitter @sjoshiMD.

1. Claim that the Ketogenic Diet is Beneficial for Diabetes
   1. I’ve excluded non-randomized studies from this discussion for simplicity. Several short-term (<12 months), randomized studies have shown benefit (but keep reading..)
      1. Westman et al.
      2. Saslow et al.
      3. Saslow et al.
   2. As time goes on, the benefit of the ketogenic diet decreases as manifested by a decreasing net difference in glycosylated hemoglobin A1c levels (see table below)
      

      Trial	Duration	Mean Reduction of HbA1c on Ketogenic Diet	Mean Reduction of HbA1c on Control Diet	Difference in Mean HbA1c Between Diets
      Westman et al. 2008	24 weeks	1.5%	0.5%	1.0%
      Saslow et al. 2017	32 weeks	0.8%	0.3%	0.5%
      Saslow et al. 2017	52 weeks	0.5%	0.2%	0.3%

   3. Finally, further illustrating the point of the decreasing difference between glycemic levels as time goes on (likely a result of difficulty of complying with the diet and lack of any effect on the pathophysiology of diabetes), a meta-analysis of randomized-controlled trials lasting a year did not show any benefit in fast plasma glucose or glycosylate hemoglobin levels
      1. Bueno et al.
   4. What is the point to the diet if there is no benefit to it over the long-term for diabetes?
2. Claim that the Ketogenic Diet is Beneficial for Obesity
   1. Meta-analysis of randomized controlled trials lasting more than a year showed a 0.91 kg (95% CI -1.65, -0.17), which is equivalent to 2 pounds of additional weight loss compared to a low-fat strategy
      1. Bueno et al.
   2. The claims of abundant weight loss are not substantiated with high-quality research
   3. What is the point to the diet if there is only 2 pounds of weight loss after one year?
      1. To put this in perspective, this is the amount of weight you would lose if you ate 19 less calories per day for an entire year (roughly).
3. Mutation Among Inuit to Avoid Ketosis
   1. The Inuit of the Arctic consumed a diet high in fat given their dependence on marine mammals with blubber and high amounts of adipose tissue. One would expect that this type of diet, given the lack of carbohydrates, would induce ketosis. However, the Inuit of Greenland and Canada actually have a mutation to avoid ketosis.
   2. The mutation can have deleterious consequences if the Inuit are not able to obtain energy from other sources since ketone bodies are a source of energy. Unsurprisingly, the mutation increases the risk of hypoketotic hypoglycemia, which increases the risk of death, especially in infants.
   3. The plot thickens: Despite the deadly risks of the mutation, more than 80% of Greenland and Canadian Inuit have the mutation. Why? Why would evolution favor the propagation of a deleterious mutation? The only reason is if the alternative was worse.
   4. Some have theorized that ketosis is not likely a wise a long-term strategy for survival. The ketogenic diet can cause metabolic acidosis (see below) from the production of acidic ketones, which lowers the pH. In times of stress (like illness, trauma, starvation, cold weather?, etc.), the blood can become even more acidic (lower pH) and increase the risk of death. Situations like this might have favored the spread of a mutation to circumvent ketosis in the Inuit.
4. Claim that the Ketogenic Diet Drastically Increases Metabolism
   1. Keto enthusiasts often tout the diet as unique because of its ability to significantly increase the metabolic rate. Not only is this not true, in some cases, it is actually the opposite of what was found in scientific studies.
      1. When ketogenic and non-ketogenic low carbohydrate diets were compared to each other, there was no difference in metabolism.
      2. Researchers at the NIH have shown that low-fat diets (like a whole-foods plant-based diet) actually result in more fat loss than low-carb diets (e.g. the keto diet).
         1. The low-carb diet did lose more total weight but this study shows that this weight was from lean tissue (muscle) loss and water loss, and not loss of fat (the opposite of what is generally desired).
         2. Other studies have also shown the sizable amount of water lost with the ketogenic diet, which is regained once the ketogenic diet is stopped.
      3. It has been hypothesized that the ketogenic diet can increase energy expenditure by a whopping 400-600 calories per day. In a scientific study, researchers found that the increase energy expenditure in the ketogenic diet was much smaller and approached the limit of science to detect the increase. In addition, fat loss was less compared to those on a high-carb diet. Finally, those eating a ketogenic diet had more water and lean body mass loss than those eating a low-fat, high-carb diet.
5. Documented Side Effects of the Ketogenic Diet from the Pediatric Epilepsy Literature
   1. Arrhythmias
      1. Best et al.
      2. Freeman et al. 1998
   2. Bone Disorders
      1. Decreased Bone Mass without Fracture
         1. Bergqvist et al. 2012
         2. Hahn et al.
         3. Kang et al.
         4. Mackay et al.
      2. Skeletal Fractures
         1. Bergqvist et al. 2007
         2. Groesbeck et al.
   3. Cardiomyopathy
      1. Best et al.
      2. Kang et al.
   4. Carnitine Deficiency
      1. Mackay et al.
      2. Peterson et al.
      3. Rios et al.
   5.  Constipation
      1. Groesbeck et al.
      2. Kang et al.
      3. Mackay et al.
      4. Rios et al.
      5. Vining et al. 1998
      6. Coppola et al.
   6. Cholesterol Abnormalities (Elevated triglycerides, elevated LDL, elevated apolipoprotein B, and/or decreased HDL)
      1. Ballaban-Gil et al.
      2. Bergqvist et al. 1998
      3. Bergqvist et al. 2012
      4. Chesney et al.
      5. Dekaban
      6. Groesbeck et al.
      7. Kang et al.
      8. Kwiterovich et al.
      9. Mackay et al.
      10. Nizamuddin et al.
      11. Rios et al.
      12. Vining et al. 1999
      13. Coppola et al.
      14. Suo et al.
      15. Retterstol et al.
   7.  Death
      1. Bank et al.
      2. Groesbeck et al.
      3. Kang et al.
      4. Stewart et al.
   8.  Dehydration
      1. Kang et al.
      2. Wheless
   9. Gastrointestinal Disturbance (Nausea, Vomiting, Diarrhea)
      1. Bergqvist et al. 2012
      2. Freeman et al. 1998
      3. Kang et al.
      4. Mackay et al.
      5. Rios et al.
      6. Vining et al. 1998
      7. Coppola et al.
      8. Galvan et al.
      9. Suo et al.
   10. Hematologic Disturbances (Anemia, Bone Marrow Suppression, Neutropenia, Platelet Dysfunction)
       1. Ballaban-Gil et al.
       2. Berry-Kravis et al.
       3. Chin et al.
       4. Goodwell et al.
       5. Kang et al.
       6. Rashidian et al.
       7. Suo et al.
   11. Hepatic Dysfunction
       1. Ballaban-Gil et al.
       2. Kang et al.
       3. Suo et al.
       4. Freeman et al. 2006
   12. Hypoglycemia
       1. Kang et al.
       2. Mackay et al.
       3. Rios et al.
       4. Coppola et al.
   13. Hyponatremia
       1. Kang et al.
   14. Hypoproteinemia
       1. Ballaban-Gil et al.
       2. Kang et al.
       3. Suo et al.
   15. Hypercalciuria
       1. Mackay et al.
   16. Hyperuricemia
       1. Kang et al.
       2. Suo et al.
   17. Infections (Non-Pneumonial)
       1. Kang et al.
       2. Vining et al. 1998
       3. Coppola et al.
       4. Suo et al.
   18. Kidney Stones
       1. Bergqvist et al. 2012
       2. Freeman et al. 1998
       3. Furth et al.
       4. Groesbeck et al.
       5. Hemingway et al.
       6. Kang et al.
       7. Kielb et al.
       8. Livingston
       9. McNally et al.
       10. Rios et al.
       11. Sampath et al.
       12. Suo et al.
   19. Lack of Appetite (Hyporexia/Refusing Food)
       1. Rios et al.
       2. Coppola et al.
       3. Suo et al.
   20. Lipemia Retinalis
       1. Livingston
   21. Metabolic Acidosis
       1. Best et al.
       2. Freeman et al. 1998
       3. Rios et al.
       4. Kang et al.
       5. Vining et al. 1998
       6. Coppola et al.
       7. Suo et al.
   22. Mineral Deficiencies
       1. Calcium
          1. Bergqvist et al. 2007
          2. Hahn et al.
          3. Zupec-Kania et al.
          4. Suo et al.
       2. Chromium
          1. Zupec-Kania et al.
       3.  Copper
          1. Chin et al.
          2. Goodwell et al.
          3. Rashidian et al.
          4. Zupec-Kania et al.
       4.  Iron
          1. Kang et al.
       5. Magnesum (Hypomagnesemia)
          1. Kang et al.
       6.  Manganese
          1. Zupec-Kania et al.
       7.  Molybdenum
          1. Zupec-Kania et al.
       8.  Phosphorus
          1. Bergqvist et al. 2007
          2. Zupec-Kania et al.
       9.  Selenium
          1. Best et al.
          2. Chee et al.
          3. Zupec-Kania et al.
       10.  Zinc
           1. Bergqvist et al. 1999
           2. Zupec-Kania et al.
   23. Optic Neuropathy
       1. Hoyt et al.
   24.  Pancreatitis
       1. Kang et al.
       2. Mackay et al.
       3. Stewart et al.
   25.  Pneumonia
       1. Freeman et al. 1998
       2. Kang et al.
   26. Prolongation of QT Interval
       1. Best et al.
   27. Restricted Growth
       1. Bergqvist et al. 2007
       2. Bergqvist et al. 2012
       3. Groesbeck et al.
       4. Hemingway et al.
       5. Mackay et al.
       6. Peterson et al.
       7. Vining et al. 2002
       8. Williams et al.
   28. Vitamin Deficiencies
       1. Biotin
          1. Zupec-Kania et al.
       2. Folate
          1. Zupec-Kania et al.
       3.  Niacin
          1. Zupec-Kania et al.
       4. Pantothenic Acid
          1. Zupec-Kania et al.
       5.  Riboflavin
          1. Zupec-Kania et al.
       6.  Thiamin
          1. Zupec-Kania et al.
       7. Vitamin B1
          1. Hoyt et al.
       8. Vitamin B6
          1. Zupec-Kania et al.
       9. Vitamin C
          1. Zupec-Kania et al.
       10. Vitamin D
           1. Bergqvist et al. 2007
           2. Hahn et al.
           3. Zupec-Kania et al.
6. Harms of Low-Carbohydrates Diets in General
   1. Birth Defects (Neural Tube Defects)
      1. Desorsiers et al.
   2. All-Cause Mortality
      1. Fung et al.
      2. Lagiou et al.
      3. Li et al.
      4. Noto et al.
      5. Seidelmann et al.
      6. Sjögren et al.
      7. Trichopoulou et al.
      8. Global Burden of Disease Study 2016
         1. Largest dietary risk factor for death is a diet low in whole grains
         2. Of note, previous years have shown similar results
   3. Cancer Mortality
      1. Fung et al.
      2. Trichopoulou et al.
   4. Cardiovascular Mortality
      1. Fung et al.
      2. Lagiou et al.
      3. Li et al.
      4. Sjögren et al.
      5. Trichopoulou et al.
   5. Coronary Artery Calcification
      1. Snell-Bergeon et al.
   6. Cardiovascular risk factors
      1. Mansoor et al,

If you have other studies or comments, please post them below in the reply section of this page. You can also share them with me on Twitter @sjoshiMD.

Last Updated 11/4/18

I wrote this article for a senior Indian-American audience in Upstate New York. I share it here as the main points are applicable to all of my readers, regardless of age or ethnicity.

Kidney disease is no stranger to Indians. It affects nearly 1 in 10 people in India and even a higher number for those who come to America. The high rate of kidney disease is thought to be due to the higher rates of high blood pressure and diabetes in our demographic. Because of this, it is important to take an active approach to preventing, treating, and reversing these diseases, especially as they relate to kidney disease. Once your kidneys are gone, the options become limited.

Diabetes

Diabetes takes its toll on every part of the body with the kidneys being no exception. Diabetes is the number one cause of kidney failure for both Americans and Indian-Americans, but diabetes occurs at a higher rate in the Indian community than the average American due partly to our propensity for developing the disease and mostly to our dietary habits that include foods high in sugar, fat, and calories; gulab jamun may be tasty, but it isn’t particularly healthy. Up to a third of patients with diabetes don’t know they have it, which is why it is important to be screened periodically, especially if you are overweight. For those afflicted, it is important to lose weight, exercise daily, and eat a diet with plenty of fruits and vegetables. These recommendations also apply to the second most common cause of kidney failure: high blood pressure.

High Blood Pressure

High blood pressure, or hypertension, puts a strain on the kidneys causing scarring and damage over the years. Like diabetes, many with high blood pressure don’t know they have it–up to half of those affected. Checking your blood pressure can easily be done at a doctor’s office, a health fair, or at home with a portable blood pressure machine. Those who have high blood pressure should limit their salt intake along with other parts of a “bad” Indian diet, like ghee, fried foods, and sweets. Replacing these items with fruits, vegetables, lentils, and beans is crucial to having a normal blood pressure. As with diabetes, losing weight, exercising, and seeing a physician regularly can reduce your risk of kidney disease from high blood pressure.

Medicines

Any discussion of kidney disease in Indians needs to include the risk of medicines, specifically Ayurvedic medicines.  Ayurvedic medications can include heavy metals, like gold, mercury, lead, arsenic, and cadmium, all of which are particularly toxic to the kidneys. For those on Ayurvedic medicines, it is best to consult with your physician on how to avoid exposure to these heavy metals. Another danger is the class of drugs known as non-steroidal anti-inflammatory drugs (NSAIDs), which reduce blood flow the kidney and can cause damage with repetitive NSAID use. Those using NSAIDs–like naproxen and ibuprofen, among others–should minimize the use of these medications and avoid being dehydrated when they are used. Finally, if you are on medications for diabetes or high blood pressure, it is important to take them as prescribed by your doctor.

Summary

We have been blessed to have two kidneys, but, for some, two kidneys are still not enough. Too many patients end up with kidney failure, requiring dialysis or transplantation–options that are not as good as preventing kidney failure in the first place. Fortunately, for most of us, kidney failure can be prevented by avoiding the damage of high blood pressure and diabetes and using medications judiciously. By making the right decisions over a lifetime, two kidneys can be more than enough.

I recently wrote a letter to the editor to JAMA Internal Medicine on the article posted above. The editors rejected it, but I’ve posted it here for your viewing pleasure.

Dr. Curfman recently highlighted the lack of benefit of ω-3 fatty acids in recent studies, despite their initial promise, in the secondary prevention of cardiovascular disease. His editorial also mentions the American Heart Association’s recommendation that adults consume fish at least twice weekly and himself concludes with similar advice for his readers.

The consumption of fish on a regular basis was brought to the forefront because of the ω-3 fatty acids within fish oil and their presumed beneficial properties on cardiovascular health, as Dr. Curfman mentioned. However, subsequent studies, including large meta-analyses using endpoints like all-cause mortality and primary prevention of cardiovascular disease, have failed to show any benefit of ω-3 fatty acids. Additionally, one of the original studies, the DART-2 trial, even showed a statistically significant increase in sudden cardiac death with increased fish oil consumption.

The continued consumption of fish is all the more concerning given the elevated concentrations in fish of toxic substances like polychlorinated biphenyls (PCBs), mercury, lead, cadmium, and dioxins, all of which can adversely affect human health. Additionally, a meta-analysis of fish consumption has shown that a single serving of fish in the U.S. per week has been associated with an increase in the risk of diabetes, possibly from the PCBs or mercury, or both. Further, both childhood and current consumption of fish has been shown to decrease cognitive performance in older Americans, who are most likely to suffer from cardiovascular disease. Until we have strong, compelling evidence on the health benefits of fish or fish oil, it may be safer to avoid its consumption entirely or obtain fatty acids from sources with lower concentrations of pollutants, like algae.

This article was written prior to Puzder’s withdrawal of his nomination as labor secretary. I am well aware that he is no longer the nominee, but have posted the article for its points on the minimum wage and public health.

President Trump’s nomination of Andrew Puzder, the current CEO of the company that operates Hardee’s and Carl’s Jr., for labor secretary is not only a poor choice for protecting the American workforce, but also undermines important public health issues that have their roots within the fast-food industry. Puzder has notoriously opposed increases in the minimum wage and paid sick leave, both of which have impacts on healthcare at a national level.

Addressing the economic pitfalls of a minimum wage hike is the first step in addressing the public health concerns associated with minimum wage workers, as any public health measure will likely not take hold if it is thought to be financially untenable. Puzder has tritely argued that raising the minimum wage will reduce jobs, slow the economy, and hurt workers, when, in reality, none of which have actually happened during the nearly two dozen times the minimum wage has been increased. Ironically, the Department of Labor’s own website features a “Minimum Wage Mythbusters” webpage debunking common arguments against any federally mandated pay increase, which might be of benefit for Puzder to read for the office he may soon take over–at least before it disappears like other federal websites unfavorable to the new administration.

Not only have increases in the minimum wage created jobs in most cases, but they have also been shown to improve health outcomes. In a 2014 analysis examining the effects of a wage increase in California, researchers found that increasing the minimum wage would decrease the rates of hunger, smoking, obesity, premature death, depression, and bipolar illness. The results are not surprising as minimum wage workers are living paycheck to paycheck and any additional disposable income might then be used towards important health-related costs, including food, medications, and copays.

Unsurprisingly, minimum wage fast-food workers depend heavily on public benefits, like Medicaid, food stamps, and the earned income tax credit. According to a 2013 study by the Center for Labor Research and Education at the University of California-Berkeley, fast-food worker subsidies amount to nearly $7 billion a year–of that, of which an estimated $247 million goes to the workers of Puzder’s Carl’s Jr. and Hardee’s annually. A raise in the minimum wage could translate into savings of billions of dollars that could be used for other government services, like other public health measures.

Raising the minimum wage seems like the obvious choice when considering the cost to consumers: only two cents to every burger purchased for every dollar added to the minimum wage. Thus, raising the minimum wage by two dollars would add less than a nickel to a Hardee’s Thickburger.

Another seemingly obvious public policy measure is giving restaurant workers paid sick-leave when they are sick. Restaurant workers, who are already stretched thin, shouldn’t be compelled to work during illness for fear of financial ruin. The Centers for Disease Control estimates that nearly 48 million people–1 in 6 Americans–are sickened by a foodborne illness each year, with 60% of outbreaks starting within restaurants. Having a restaurant worker be sick, it turns out, is the single most common cause of an outbreak, which can be mitigated by having paid sick-leave for workers. It’s a policy Puzder might have already taken note of: In 2015, more than 3,700 people were treated for possible exposure to a foodborne illness after eating from two South Carolina Hardee’s where one of the employees was infected with Hepatitis A.

Puzder’s nomination for labor secretary reminds us of George Orwell’s concept of doublethink–where the offices entrusted with protecting us may actually be hurting us. It may be one reason why so many of Hardee’s and Carl’s Jr. employees have protested his nomination. In addition to being anti-labor, his policies are decidedly anti-health, which is why the Center for Science in the Public Interest has also decried Puzder’s nomination. Lest anyone had forgotten the obvious, Puzder’s Hardee’s is the home of the 2/3rd pound Monster Thickburger, a dietary abomination with 1,340 calories, 96 grams of fat, 34 grams of saturated fat, 275 grams of cholesterol, and 3,130 grams of sodium. To say the least, Thickburger policy will not be making anyone healthier under Puzder’s reign.

In my latest post, I discuss the recent decline in life expectancy in America and one possible way we might be able to combat it.

“Wrong” (original) by Raul Lieberwirth is licensed under CC BY-NC-ND 4.0

 

There has been on average one mass shooting (involving at least 4 people) for every day this year. In the wake of the San Bernardino shooting – the most recent widely-covered mass shooting, America has reopened the debate over gun control, pitting a bereaved public beckoning for gun reform against rifle-thumping, strict-Constitutionalists. Yet, in this polarizing debate filled with a seemingly binomial future, there are other options: namely those that focus on common-sense public health measures, like repealing the federal ban on gun research and physician gag laws.

Guns kill more than 33,000 people a year. Guns kill more than double the number of Americans compared to AIDS each year. With such a heavy toll, gun-related deaths are epidemic in America. As with any other epidemic, one would expect the federal government to fund research on the causes and treatments of such a scourge on society – except with the case of guns. Since 1997, the Centers for Disease Control and Prevention (CDC) has been explicitly prohibited by Congress from using taxpayer dollars to study something that kills more than 90 people a day. As described in an article in the Journal of the American Medical Association after the 2012 Sandy Hook massacre, the action stems from an irrational fear that saving lives is equivalent to forfeiting essential American values – the act is reminiscent of 1950’s paranoia where a glance askew was labelled as McCarthyism.

All efforts to have a meaningful impact on gun violence have been dead in the water for nearly two decades. More importantly, it has left the public without any “position” statements – guidelines that set the rhetoric for public health measures – to steer the public on safety. Instead, we are left to decide for ourselves, or worse, be swayed by an increasingly emotional debate on gun safety. If you’re confused if having more guns makes America safer or more dangerous, you should be. Here’s a study showing that guns increase crime, and here’s another showing the opposite. It would be nice if the CDC – with all of their resources – could separate the noise from the signal for us.

Another counterintuitive and inane bulwark of the pro-gun group is the institution of so-called “gun gag” laws. Florida was the first, and likely not the last, state to seemingly ban physicians from asking their patients if they owned a gun and if that gun was secured and out of reach of children. Although conversation on the topic is permitted if it is “medically relevant,” many physicians find the laws so restrictive that they chill any discussion on gun safety. Such seemingly common sense practices – practices that are routine for physicians – are now banned as a part of the hysteria that envisions British red coats returning America to the Queen. If my patient finds my questioning not “medically relevant” – even though it may be, I could be liable under Florida law.

Accidental injury from guns among children is a serious issue. A 2013 New York Times article estimated gun accidents may be in the “top five or six” leading causes of unintentional deaths among children due to discrepancies in accidental death reporting. Several months ago, Darnal Mundy, a 3-year-old boy in Miami, FL, shot himself in the head while looking for an iPad. He had climbed onto a chair, reached into a drawer, found a gun, instead of an iPad, and shot himself in the head. After being in a coma for several weeks, Darnal survived and was released from the same hospital at which I work. But not all children are so fortunate, one study has estimated that nearly two children die every week from unintentional shootings alone.

According to the Children’s Defense Fund, more than 40% of gun owning households with children store their guns unlocked. Some of these households don’t know the basics of gun safety, and they may never know now given the emergence of gun gag laws. Safe storage of guns – another common sense public health measure – is supported by the American Academy of Pediatrics because it has been shown to be effective at reducing injuries. It is no surprise that the National Rifle Association, one of the most powerful lobbies in Washington, has opposed safe storage laws for guns because it would have rendered homeowners “defenseless and given criminals a clear advantage in home invasions.” I didn’t realize that locked guns had adversely affected public health so much that we should only keep guns unlocked.

Changing public health policy usually begins with solid research. If you are interested in reducing the number of preventable deaths and injuries from guns, you can begin by opposing the nonsensical ban on federal funding of gun violence research. If you are a non-physician, you can show your support here. If you are a physician, you can sign a similar ban here.

“Butchered Bacon” by Cookbookman17 is licensed under CC BY-SA 4.0

Several weeks ago, the World Health Organization (WHO) released its report condemning processed meat as a Group 1 human carcinogen – a classification that includes such notorious companions as tobacco smoking, smokeless tobacco, and second hand smoke. This is not surprising considering that processed meat contains many of the same known or probable carcinogens as cigarette smoke, like heterocyclic amines and N-nitrosamines. Red meat was labelled in the runner up category as a “probably causing cancer” – specifically colorectal cancer. The similarities between meat and tobacco also extend to how both of their industries have decried prestigious health organizations as they have issued reports aimed at improving public health and saving lives. Akin to the tobacco industry’s response several decades ago, the meat industry – using many of the tactics of Big Tobacco – swiftly denounced the WHO report.

Crying Foul

The first defense brandished by tobacco industry after the Surgeon General declared that cigarette smoking causes lung cancer in 1964 was denial. It was their most important tactic, and it served them well for decades. The industry maintained its position by creating doubt among the public. As a tobacco industry stated after the Surgeon General’s indictment on smoking, “Doubt is our product.” By creating controversy, the tobacco industry was able to defer a smoker’s need to quit smoking and preserve profits – at least until the “controversy” was settled, which took nearly three decades. In reality, among the public health community, there was never a controversy – only the one fomented by industry. At the time of the Surgeon General’s report, the average American smoked a half pack per day. Although smoking rates declined in the ensuing decades, the decline was mitigated by the industry’s aggressive tactics.

Borrowing a precedent set by the tobacco industry, the meat industry categorically denied the WHO’s landmark statement, calling it “dramatic and alarmist overreach.” The North American Meat Institute wasted no time in denying that meat causes cancer, arguing that “numerous studies” have shown “no correlation between meat and cancer.” By “numerous” they mean nine studies. In comparison, the WHO looked at more than 800 studies, from which they concluded that processed meats do cause cancer – a similar conclusion was reached by the American Institute for Cancer Research and the World Cancer Research Fund International after reviewing 7000 studies a few years ago.

Correlation is Not Causation and Other Fallacies

The industries’ best strategy to buttress their claims of denial is to argue that correlation is not causation. Simply put, just because both meat consumption and colorectal cancer rates are high doesn’t mean they are related. The industry will say that meat eating countries have a lot of power lines, for example, that could also be a cause. These are half-truths distorting basic statistical concepts to support an a priori claim. The reason the WHO concluded that processed meat cause cancer was because they looked at a wide body of evidence from multiple sources. They looked at evidence from animal studies, basic science research, and, of course, humans to see the whole picture. It was the totality of the evidence that led the WHO to eschew bacon.

It was the same approach that led public health authorities to rethink our relationship with cigarettes, which was made public with the Surgeon General’s report in 1964. In order to subvert the medical establishment, the tobacco industry created the “Tobacco Industry Research Committee” and several other decoy organizations with the express purpose of fostering claims that cigarettes do not cause cancer. These organization were filled with for-hire publicists, scientists, and physicians. In an example of organized knavery, they argued that heavy smoking was unrelated to rising rates of lung cancer and other causes were to blame – like air pollution, smoke, and automobile exhaust. We now know that smokers are 15 to 30 times more likely to get lung cancer or die from lung cancer than nonsmokers.

Examples of overt obfuscation have also occurred after WHO report debuted. House Republican and Agricultural Committee Chair Michael Conaway boorishly stated, “These claims are based on a biased selection of studies performed by an organization notorious for distorting and misconstruing data …” Although Mr. Conaway does not have any formal back ground in the medical sciences or statistics, he has received more than $350,000 in campaign support from the livestock industry, according to the Center for Responsive Politics.

In reference to the WHO’s report, the North American Meat Institute also did not mince its criticism, stating, “They tortured the data to ensure a specific outcome.” The diction is ironic and distasteful considering that the meat industry itself has been repeatedly accused of torturing animals in the process of making meat, as this PETA exposé narrated by Paul McCartney graphically illustrates.

 Benefits Outweigh the Risks

 Perhaps the only endorsement the meat industry can make at this point is one that appeals to popular conception: meat has a lot of protein (and that protein is good for you). In fact, that is exactly what the meat industry did: “Meat is ‘nutrient-dense’ and vital humans… Meat is a complete protein, meaning it contains all the amino acids our bodies need.” Yet, there are plenty of protein sources that are carcinogen-free, like beans, lentils, and tofu. In a land of plenty, there is no reason to risk cancer for the sake of protein. As a physician, I have yet to see anyone in America with a case of true protein deficiency (known as kwashiorkor).

Hormel, one of the leading meat processors, went on further to state the benefits of these nutrients outweigh any risk, the “very important nutrients in meat far outweigh any theoretical hazard.” This rhetoric of emphasizing value and discrediting the risks is not novel to the meat industry and was pioneered by Big Tobacco.

The tobacco industry used similarly deceptive advertisements throughout the 20^th century to trumpet the benefits of smoking. These advertisements feature physicians whole heartedly endorsing cigarette smoking. As recently as 1988, the then CEO of Philip Morris, Joseph Cullman III, has been caught on record trying to discredit studies showing hazard to health by stating, “There is only a statistical association. It has never been proven.”

Quantifying the Risk

The meat and tobacco industry have a self-interest in preserving their profits, but you have also have an interest in preserving your own health. The choice to smoke or consume processed meat is an individual one, but should be made based on knowing all the facts. With both of these habits, we now can quantify our risk. With smoking, we know that cigarettes cause 1 death for every million smoked. When we consider that trillions of cigarettes are smoked every year, it is no surprise that cigarettes are predicted to cause nearly a billion deaths in the 21^st century.

With processed meat, the WHO report estimates an 18% increased risk of colorectal cancer for every 50 grams per day of processed meat consumed – the amount of meat in a regular hotdog. In one large summary study reviewed by the WHO, the risk was seen to increase linearly with increasing consumption until one ate 140 grams of processed meat per day.

In America, nearly 5% of individuals will develop colorectal cancer over their lifetimes. It is the second leading causes of cancer-related deaths and the third most common type of cancer in men and women. The cancer is so common that the government recommends every adult over the age of 50 to be regularly screened for colorectal cancer. With statistics like this, it is hard to ignore the WHO’s conclusions.

The WHO estimates that 34,000 cancer deaths per year across the globe are attributable to eating processed meat. Although this number is smaller compared to the damage inflicted by cigarettes, it is still a significant issue to those getting colorectal cancer from eating processed meat. Whether its cigarettes or bacon, it is prudent to think about what we put in our mouths.

Several years ago, when I was only a first year medical student, I started out on a research project to find out why so few patients – specifically minorities – with kidney failure end up getting a kidney transplant. Research abounds on the topic, but we went ahead anyways mostly to flesh out details on minority care and to have solid proof that the problem exists in our own backyard. Our findings were eventually published in Transplantation – a respectable journal in the field.

At the end of our article, we thought about writing a familiar refrain: more research is needed on the subject to better understand it. But we didn’t. Our findings only added to an already sizable body of knowledge about a known problem; doing more research wasn’t going to solve it. Sure – additional research may be beneficial, but it would have come at a cost and may have only been marginally helpful. Given finite resources, as certainly within medicine, every action is subject to an opportunity cost; in the case of additional research, the opportunity cost could be taking those same resources and using them towards an intervention. Additional research is also subject to decreasing returns to scale. In other words, our findings weren’t as useful as the first person to ever describe it. And additional papers may not be as helpful as ours, unless they add some twist that has not previously been looked at (like minority care, as in our case).

Instead, we ended our article writing, “… more extensive educational campaigns … may allow a greater patient access to preemptive waitlisting and … transplantation.” Still we didn’t feel this was enough. Our paper showed that even in our own community patients were actively receiving substandard care. Only a few patients were being transplanted before starting dialysis (avoiding dialysis all together is the best). And, a large number of patients – specifically minorities – were spending months – even years – on dialysis (if you can’t avoid going on dialysis before a transplant, keep it as short as possible). So, we decided to implement an “intervention”.

Selecting an “intervention” and translating it into a final product was not easy and took years (for some perspective, I am now a third year resident). With the help of $15,000 in funding and skills from our transplant center, we made a trilingual video to educate end stage renal disease patients in the South Florida community about the benefits of a transplantation and how they can get one. Educating patients is usually a safe bet in terms of improving care. However, skeptics may want additional research showing that education works, which can be helpful but can also consume precious resources that could otherwise be used toward an intervention. Not that we needed it, but a paper published showed that making patients aware about kidney transplantation – as anyone would guess – increases awareness about kidney transplantation.

Our videos are available on YouTube in English, Spanish, and Creole to cater to the large number of Hispanic and Haitian patients with kidney disease in our community. Although the videos provide information specific to South Florida residents, we encourage others throughout the world to use them to deliver the main message about the benefits of transplantation. Collectively, the videos have a limited number of views at the moment, but we hope this number grows.

We also hope that these videos are an inspiration to others to effect practical change in other areas of medicine that so urgently need physician leadership and action. Additional research is always helpful, but is subject to decreasing returns to scale and opportunity costs. Sometimes, the best course may be turning those research findings into actionable change – even if you are only a medical student.

Acknowledgments: This project would not have been possible without the important contributions from Dr. Alayn Govea, Wei Yang, Hadi Kaakour, Dr. Giselle Guerra, Dr. Warren Kupin, Dr. Gaetano Ciancio, Dr. Oliver Lenz, Novartis, the Miami Transplant Institute, the University of Miami, and Jackson Memorial Hospital.