Food and Health.

This won’t be an all-inclusive blog posting. To be all inclusive would require a novel, or at least novella, length blog post. People who have read earlier blog posts will know that I’m a fan of people eating healthy and not a huge fan of “fad diets”. The best healthy diet is the one you can adhere to.

As I’ve mentioned in other posts, and can be found online, diet and other lifestyle options can affect one’s chances of developing various chronic diseases. Though in this post I’ll be limiting myself to diet, and just a few things about it as well – and save other comments and suggestions for another time.

One piece of advice I can remember getting is to make sure one’s plate (ok, the food on one’s plate) is colorful as in having a lot of different colors. Granted in some cases (carrots and spinach) the colors don’t really indicate that they’re both high in the Vitamin A precursor Beta – Carotene, but both are (and have different profiles of how much of other healthy vitamins and fiber they have). Making sure that there are differently colored foods also means you’re likely to get other benefits. Both blueberries and cherries have a lot of antioxidants in them which can affect health. Though I think that we tend to look at their antioxidant effects too much at the expense of other effects they might have, such as on sugar absorption and metabolism. Never mind that blueberries and cherries also contain some fiber. There is growing evidence that blueberries can help prevent/treat type 2 diabetes. This doesn’t mean, however, that eating them replaces medications such as metformin, acarbose, rosiglitazone, and many others. Cherries may carry a similar benefit.  Tart cherries are touted to have anti-inflammatory effects and might help reduce the need for non steroidals in some people.

The fatty acids one eats can also affect health profoundly. The N-3 (also known as omega-3) fatty acids not only help protect against heart disease, but also seem to have a role in preventing depression and helping treat it as well. Though depression as an inflammatory mediated illness has gotten some press (though at the moment I don’t have a reference for that, and who hasn’t felt miserable when (s)he has a cold or the flu), it also avoids the fact that N-3 and N-6 fatty acids also get incorporated into cell walls, including nerve cells. This incorporation also affects the fluidity of the cell walls and therefore how well receptors work as well as how easily (or hard) nerve cells release neurotransmitters.

My advice, as always, is to try to avoid getting vitamins and such through supplements for a few reasons:

  1. In some cases they can do more harm than good (especially true of fat soluble vitamins). In one study, smokers that took vitamin A supplements had higher rates of lung cancer than those that didn’t.
  2. You might not be getting all the relevant forms of particular vitamins. For example, there are different forms of vitamin K, some promote clotting, others bone health.
  3. With a varied diet, one can get enough vitamins and antioxidants without supplements. You have to eat anyhow, even if you buy pills.

There are several times, however, where it might be worthwhile. For example:

  1. If you have had a gastric bypass, or a stomach resection for another reason, taking supplemental B12 is important so as to keep stores normal.
  2.  If you have a disease, or take a medication, that interferes with absorption of particular vitamins (Crohn’s and other diseases that affect the ileum can interfere with absorption of B12, anti ulcer mediations do the same.)

I’ve talked about diet before (The Pantry Prescription) so I won’t go into it today. I may do an updated version of  that post in the future.

Anyhow, here are some references to a few of the things I’ve mentioned today:

Coultrap, S. J., Bickford, P. C. & Browning, M. D. Blueberry-enriched diet ameliorates age-related declines in NMDA receptor-dependent LTP. Age (Dordr) 30, 263-272 (2008).

Ren, T., Zhu, J., Zhu, L. & Cheng, M. The Combination of Blueberry Juice and Probiotics Ameliorate Non-Alcoholic Steatohepatitis (NASH) by Affecting SREBP-1c/PNPLA-3 Pathway via PPAR-α. Nutrients 9, (2017).

Stull, A. J. Blueberries’ Impact on Insulin Resistance and Glucose Intolerance. Antioxidants (Basel) 5, (2016).

Lee, Y. M. et al. Dietary Anthocyanins against Obesity and Inflammation. Nutrients 9, (2017).

Mazaherioun, M. et al. Long Chain n-3 Fatty Acids Improve Depression Syndrome in Type 2 Diabetes Mellitus. Iran J Public Health 47, 575-583 (2018).

Masoumi, S. Z. et al. Effect of Citalopram in Combination with Omega-3 on Depression in Post-menopausal Women: A Triple Blind Randomized Controlled Trial. J Clin Diagn Res 10, QC01-QC05 (2016).

Grant, R. & Guest, J. Role of Omega-3 PUFAs in Neurobiological Health. Adv Neurobiol 12, 247-274 (2016).

Husted, K. S. & Bouzinova, E. V. The importance of n-6/n-3 fatty acids ratio in the major depressive disorder. Medicina (Kaunas) 52, 139-147 (2016).

Kobayashi, M. et al. Dietary n-3 Polyunsaturated Fatty Acids in Late Pregnancy and Postpartum Depressive Symptom among Japanese Women. Front Psychiatry 8, 241 (2017).

Levant, B. & Healy-Stoffel, M. N-3 (Omega-3) Fatty Acids: Effects on Brain Dopamine Systems and Potential Role in the Etiology and Treatment of Neuropsychiatric Disorders. CNS Neurol Disord Drug Targets (2018).

Pusceddu, M. M., Kelly, P., Stanton, C., Cryan, J. F. & Dinan, T. G. N-3 Polyunsaturated Fatty Acids through the Lifespan: Implication for Psychopathology. Int J Neuropsychopharmacol 19, (2016).


Evaluating health care claims

In some ways this post is a continuation of my previous one titled “…because it’s natural”. In a lot of diseases such as DM-2, Alzheimer’s, and heart disease, there are multiple mechanisms that contribute to either the disease itself or to it’s complications. Two mechanisms of disease that seem to get a lot of space on TV, print and on the internet is that of inflammation and oxidation. Whether it is someone promoting a “super food” that has a lot of antioxidants in it (or a lot of anti-inflammatory activity), or a pill that has plant extracts in it that reduce oxidation or inflammation, the claims should be  taken with a grain of salt. For example in some cases, there may be multiple good studies that show taking said supplement does act as good antioxidant. However this doesn’t mean that the supplement will improve one’s health or lengthen lives. This is a problem with using what’s called a surrogate endpoint. Don’t get me wrong, using surrogate endpoints can be useful when the more significant and relevant endpoints are things to be avoided (death or disability for example) or might not happen for years  – I don’t think a study that would take 30 years to start showing something works would get funding – or finding enough people to study would be practical. It helps if a change in the surrogate endpoint has already been shown to be related to reduction in a particular disease’s morbidity or mortality.There are also observational studies that show certain things (high vitamin A levels, higher beta-carotene intake) are associated with lower levels of a particular disease state. Sometimes using a surrogate endpoint  (or  noticing an association between two things such as high levels of vitamin A and lower rates of a particular disease) ends up leading to people doing negative studies. For example, many deaths after a heart attack are related to arrhythmias. A study called the CAST (short for Cardiac Arrhythmia Suppression Trial) showed  higher mortality in people who were on anti arrhythmia drugs. It doesn’t mean that the drugs didn’t have a role in other disorders. I have a feeling it means that we were just asking the wrong question (even though it needed to be asked and answered) about treating arrhythmias after heart attacks. I use the example of the CAST study to make the point that showing something changes the level of something (either up or down) that is thought to be involved in causing disease – be it inflammation, oxidation, arrhythmia or otherwise – doesn’t mean it affects the disease it is said to. It may be that to treat a disease with anti-inflammatory medications (or substances), one also needs to block other pathways of that disease as a well for any to be effective. This is why most cancers are treated with more than one drug. This is why people are often on more than one blood pressure medication. As I mentioned in my last post, any claims should have data supporting that they work. The results should be reproducible, hopefully other by other researchers. Getting back to my original assertion from the start of this particular blog post, if someone is touting a “superfood” for health, It is appropriate to ask if it actually improves health, decreases complications, etc. In my opinion, just to say something is a “super food”  because it is a ‘super anti oxidant’ is blowing smoke.  That isn’t to say that anti-oxidant rich foods don’t promote good health. There are too many studies that are negative that to look at one thing and say “this is the holy grail of food”. This also undersimplifies things too greatly. It’s better, in my opinion, to say “these are the types of foods/eating (or habits if one is talking about other aspects of lifestyle) that are associated with good health. For examples, many of the studies that show that olive oil intake is inversely related to cognitive decline are more agnostic about what role each component in olive oil plays, despite showing benefits. Is it the kinds of fatty acids in olive oil? Is it the polyphenols that act as antioxidants?  Is it the anti-inflammatory chemicals in olive oil? I suspect the answer is yes, it is all three. Is it the answer to everything: just have olive oil and you’ll live to 100? I doubt it. My bottom line on health care claims:

Be critical but open minded: ask the following questions: “Does it actually affect or prevent disease? Does it decrease complications of the disease and not just something thought to be associated with disease or complications thereof?”. If the answer is “yes, it does reduce _fill in the blank_ and there is a proportional reduction in the amount of deaths/strokes/people going on dialysis/etc then you have a winner. IF the answer is “it does reduce _fill in the blank_” but there is no reduction in _fill in this blank as well_” it may mean that the answer is more complicated than we think. It may mean that the wrong question(s) were asked, or the right ones hadn’t been asked.

Also be wary of claims that make a product or procedure seem that it’s THE ANSWER for a particular disease. It may be a piece in the puzzle, but in order to be considered as such, the answer to the question ‘where’s the proof’ should be along the lines of “here are the studies…”

If the person makes statements like “doctors are in the pockets of ‘big pharma’ and aren’t interested in curing disease”, then be wary. I think most doctors get into this business to make people better. If there was a pill that taken once or twice cured someone of his or her type 2 diabetes (and did not cause some other severe life threatening disease), I think most doctors would use that pill.

Also ask if this the first study of something? Often a treatment is found in a study to be helpful. The numbers of people may be small. Due to the nature of studies, the participants are typically more homogenous than the population as a whole. Once larger studies are done, the benefits of a medication/procedure, etc may not be as large as initially thought.

Another question ot ask is this better than what we have now? Though it could be asked of a new medication, I’m primarily thinking here of new surgical procedures (eg, robotic surgery for certain things). If offered ask: is the rate of complications less with the new procedure? Is mortality less? Is the recovery time quicker with the new procedure?

Screening – part II

In my previous post I wrote about the kinds of screening that could be though of as what you get for having reached a certain age (eg, age 50 for colonoscopy/colon cancer screening) or age +/- behaviors (eg, a sexually active female above a certain age). In future posts I might write about a particular screening test in more depth.

However in this post I’d like to talk about screening for genetic diseases. This is a bit different that the screening I wrote about last time and people can fall into several groups. One group is to see if someone will develop a disease. One disease that fits this mold is Huntington’s Chorea. People who have the mutation do  go on to develop the disease. For Huntington’s Chorea there needs to be a clear family history for testing. For Huntington’s, as well as well as other’s like it, there are multiple things to consider before testing. A big consideration  for Huntington’s Chorea is how one would handle the information if one was found to have the disease (there is no asymptomatic carrier state the same way there is for tay sachs, sickle cell anemia and others). Either you have the mutation and will develop the disease or you don’t and won’t. Someone might choose only to get tested if there is a chance they will have kids and want to know the chances of passing the disease onto their children, or to do prenatal testing, which brings up a whole lot of other issues beyond the scope of this post (what would you do if the test was positive? would you end the pregnancy? Would you go forward knowing you and the child you bring into the world would develop the disease? Would you get tested or do prenatal testing of the child if you were against ending the pregnancy? If you get tested before pregnancy and are positive, would you decide not to have children or would you do some sort of pre-implantation diagnostic testing and then only implant embryos that are free of the disease  – this latter approach might not be something insurance covers which is a whole other discussion/set of issues). Another disorder that fits into this category is Familial Polyposis Coli.  People who inherit this disorder have a virtually 100% chance of developing colon cancer and have an average age of 39 at the time of diagnosis of colon cancer. There are a few mutations associated with this disease which give rise to a somewhat different course of disease (mainly in the average age of diagnosis, # of polyps, etc). To my knowledge the best diagnostic tests for this are family history and colonoscopy rather than genetic testing – it allows for biopsy, quantification of the # of polyps, etc). In this case testing for the disease poses fewer of the issues than say, Huntington’s as there is a treatment available for this disease. If or when there is a treatment for Huntington’s chorea, then some some of the thornier issues mentioned above change.

This brings us to the next group – screening for a carrier state. What disorders one screens/gets screened for depends on one’s family history as people from different parts of the world are at risk for different diseases. Examples of disorders I am thinking of include Sickle Cell Anemia, any of the Thallessemias (and there are several. Some are lethal if inherited. Others are lethal or more symptomatic if two forms are interited together) If one is free (as best as genetic testing can tell), one’s partner might still want to be tested. Their children might not be at risk but grandchildren might and knowing that risk can be helpful. If both partners carry the trait for a particular disease several options exist. Some I mention above (testing pre implantation genetic diagnosis, aka PGD), deciding not to have children, etc. How one might choose to use the information is a matter of conscience.

In the last group of screening, it is to assess whether one is at risk for developing diseases where family history of suggestive of high risk: testing for BRAC1 and BRAC2 mutations in people whose family history includes a high incidence of breast and/or ovarian cancer, for example. This group is similar to the first one. Family history can guide if someone’s high risk. It is unlikely a clinical geneticist would screen for Huntington’s in someone with no family history whatsoever. If the family history shows only sporadic cases of breast or ovarian cancer, for example, testing for BRAC1 and BRAC2 would be less helpful. In these cases it is the person him/herself who’s at risk for the disease.  With some tests such as for BRAC1 and 2, the risk of disease may not be 100%, as it is with Huntington’s. In cases testing, some can decide about, say prophylactic mastectomy and/or oophorectomy, whether to wait after one has had children, etc. Of note, even if the risk is for typically a “womens’ disease” and the risk is on a father’s side of the family it is worth testing for.

Some last thoughts on this issue. If one is thinking of doing any sort of genetic testing, a primary care physician is a good place to start as he or she will at least be able to give some input on how likely one has a hereditary syndrome running in the family. However for actual testing it’s better to go through a clinical geneticist for testing. They have the background to pre and post test counseling.  The clinical geneticist will also be be set up with a lab that would do the testing, as even in a tertiary care center, the laboratories that do the testing are more specialized than  those that do the routine testing physicians do.

Related articles