Posts Tagged ‘Medical research’

Vindication?: part 2

Sunday, January 8th, 2012

here's a high-protein diet

In my my previous post, I talked about my own dieting program, but mentioned a very recent article in the Journal of the American Medical Association, typically called JAMA. I came across a newspaper article on this research study while reading The Wall Street Journal . Now I want to analyze  the  JAMA article. Let me give you a quick overview and then I’ll tell you what bothers me about the implications.

Three groups of relatively young people (18 to 35) were fed extra calories with varying amounts  of protein while living in a special metabolic unit. They all gained weight, but those fed a low-protein diet gained less. That group increased their total body fat just like the others did, but did not gain “lean body mass” (that’s anything but fat: i.e., bones, organ weight and muscles), while those on a normal protein intake and those eating more protein than usual gained not just fat, but also muscle mass. So calories count more than composition of a diet, but extra calories with too little protein leads to weight gain that’s all fat (90% of those surplus calories formed fat; 10% went into the energy necessary to do so).

Okay, that’s the classic comic version. Let me dissect the study and its conclusions a bit more.

This was a relatively short-term study of what happens when people overeat.  The extra calories the subjects ate were in the form of fat. It was also a small study with only twenty-five subjects who were healthy non-smokers, weren’t allowed alcohol or caffeine and had stable weights to begin with. They varied from quite lean to overweight, but none of them were obese. It was a “single-blind” study, that usually translates to meaning a study in which either the investigator or the participant, but not both of them, is unaware of the nature of the treatment the participant is receiving; in this case only the kitchen staff knew who was in which diet group.

The research was exceedingly well done with careful methods, an inpatient ward for the study subjects, a preliminary period where diets were adjusted to keep their weight constant, and lots of state-of-the art measurements of how much fat and how much muscle each person had before and after the eight-week diet.

So far, so good: eating too much makes you gain weight; lots of that weight is fat. Eating more protein tends to add muscle (I can’t see that their bones got heavier or the basic weight of their organs, though they likely accumulated some fat).

all vegetarian food

All that makes sense to me; now how does that apply to dieting? I think it likely does, but that’s not what this study was designed to show. The question that remains is what should I eat if I want to lose weight? I just found an article in The Telegraph (a London paper I never read otherwise). The title was “Vegetarian low protein diet could be key to long life.”

Unfortunately, the study was done in fruit flies. The lead author said “…similar results have been found in mice.” Thus far a variety of studies in animals imply we can live longer by eating less. I’ll accept that, but for now, until there are large-group human studies, I’m sticking to reasonable amounts of protein and less overall calories.

 

 

What’s worse than TBI?

Friday, December 9th, 2011

play today, pay tomorrow?

In my last post I wrote about the immediate risk to our youngsters, that of traumatic brain injury (TBI). Now I’d like to move on to an even grimmer issue, much more severe and long-lasting brain damage that’s also trauma-associated. We’ve heard of professional football players developing personality changes, then more severe neurological problems; most recently I read of a professional hockey player who had similar issues.

So I found the Boston Center for the Study of Traumatic Encephalopathy (that term translates as “disease, damage or malfunction of the brain.”), and read one of their major publications on what is called Chronic Traumatic Encephalopathy   (CTE). Trust me, most of the medical jargon it uses is tough even for a Internal Medicine subspecialist. It was published in a journal I’ve never heard of, J Neuropathol Exp Neurol, but is very well written and, in addition to detailing the brain changes in 48 cases of CTE, provides an excellent background discussion of the entity. Ninety percent of the neuropathological confirmed cases of CTE were in athletes.

I remembered a story in 2009 of a 26 year old Cincinnati Bengals receiver who had died after falling out of a pickup truck during a domestic quarrel, reviewed the recent New York Times piece on a 260+ pound NHL “enforcer” who died of a combined alcohol and painkiller overdose and found another Times article, this one from May of 2011, about a former Chicago Bears defensive back who had committed suicide and donated his brain to the Boston research center. All three had CTE.

That article said about two dozen retired NFL players were eventually found to have this disease; the research article mentions that over one-sixth of those having repetitive brain injuries called concussion or mild TBI eventually will go on to have CTE .

But we’re not just speaking of football players or hockey players. Professional wrestlers, soccer players, domestic abuse victims, military veterans, horseback riders, seizure victims, head bangers as well as boxers and hard-form martial arts participants may well have similar recurring brain trauma and potentially could go on to CTE.

It's time to study their brains, hopefully before it's too late.

The NFL donated $1 million in 2010 to CSTE, the Boston University research group; researchers at the center have lined up 100 former players  to try to find ways to diagnose the condition during life and more than 250 active and retired NFL players have agreed to donate their brains and spinal cords to the CSTE.

Nearly 100 are suing the league over the issue of player safety, saying the NFL has down-played the concussion problem to give fans more action. A knowledgeable friend told me the NHL allows bare-fisted fights between its enforcers and others to go on for roughly fifteen seconds; he said the audience loves the brutality.

Bread and circuses were a way to keep the Roman populace from revolting. Why are we emulating them?

 

 

It goes far beyond football, boxing and hockey

Wednesday, December 7th, 2011

The brain is vulnerable to trauma

I feel like I’ve opened the proverbial can of worms, finding, in this case, a topic that keeps expanding. I started with reading an article in The New York Times about the death of a professional hockey player, but I quickly delved into the medical literature.

I’ve spent much of the day reading article after article on traumatic brain injury  (TBI), which can be mild or severe, and another entity called chronic traumatic encephalopathy or CTE, one that’s frequently been in the news over the last two years. Let’s start with TBI. I’ll be writing about teens and younger kids. I’ll deal with CTE in another post focused on adults.

A Center for Disease Control and Prevention (CDC)  report in the most recent edition of the Journal of the American Medical Association reviewed nonfatal TBI related to either sports or recreational activities in kids age 19  or younger. The numbers involved were staggering, nearly 175,000 per year being seen in Emergency Departments (EDs).

A large majority of those sports and recreation-related TBI ED visits were by boys and the annual total of those ED trips increased markedly during that nine-year time frame. They were injured biking, playing football, soccer, basketball or while engaging in miscellaneous playground activities. They went to the ED in smaller numbers for injuries suffered in many other activities, including horseback riding, ice skating, ATV riding, tobogganing and even golfing (here the injuries included those related to golf carts). Surprisingly, skateboarding accounted for only a fourth of the ED visits for biking and football accidents and TBI was less frequently seen.

A helmet is a good start

As my wife and I drive around town, we often see college students riding their bikes at night while helmet-less and light-less. I fear for their brains.

There’s another, less well-accepted entity, so-called “Second Impact Syndrome.” I read an article about this in a February 2009 article by two authors on the faculty of the University of California, Irvine School of Medicine. In this scenario athletes who’ve had a TBI then have a second brain injury when they go back to playing their sport far too quickly. The initial injury may have been relatively mild; the recurrent trauma may kill them in a matter of minutes.

Another review of this  syndrome said 94 catastrophic head injuries had been reported in American high school and college football players in a 13-year time frame, 92 in high schoolers.  Seven of ten had a prior concussion in the same football season; over a third played with continuing symptoms.

This speaks to the crucial question of when an athlete (or a bike or horseback rider) who has suffered TBI should return to their sport/activity. Last night I called a younger friend who had been bucked off his spooked mare and suffered a concussion eight days ago. He was still having headaches and agreed with me that it was far too soon to get back on his horse.

A new CDC program called Heads Up offers TBI guidelines for coaches, parents and physicians.

 

 

 

So is it your thyroid after all?

Wednesday, November 30th, 2011

Is this woman depressed, hypothyroid or both?

On November 21, 2011, The New York Times had an article entitled “For Some, Psychiatric Trouble May Start in Thyroid.” As a mental health therapist who is hypothyroid, my wife has a particular interest in this subject and pointed out the article for me.

The premise, put forth by Dr. Russell Joffe, a New York psychiatrist, and a group of his professional peers, is that subclinical hypothyroidism may play a significant role in depression. A Brown University professor of psychiatry and human behavior also commented on this connection asking, “Is there an underlying thyroid problem that causes psychiatric symptoms, or is it the other way around?

From the endocrinology side, Dr. James Hennessey, at Beth Israel Deaconess Medcsl Center in Boston, noted “Psychiatric symptoms can be vague, subtle and high individual.”

A study, published five years ago by Chinese researchers, gave six months worth of  thyroid hormone replacement therapy (see links below for the NIH’s info sheet on this medication, levothryroxine and other info from MedicineNet.com), to patients with subclinical hypothyroidism and found improvements in brain scans, memory and executive functions.

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0000684/#

http://www.medicinenet.com/levothyroxine-oral/article.htm

sketch of the thyroid gland

So how is this condition diagnosed? and what does your thyroid do anyway? Most of us are familiar with this two-lobed, twenty to sixty gram,two-inch structure, located in the front of our necks and wrapped around our windpipe. It’s a hormone producing gland with two products, thyroxine or T4 and its active hormone, triiodothyronnine or T3. I’ve always thought of its function as a major regulator of metabolism, but in reality that’s only one of its duties: it does control how speedily we use energy, but also has a role in how we make proteins, how we react to other hormones and how our bodies handle calcium.

I’ve spent much of today reading about the thyroid; some things I knew; some I hadn’t reviewed since med school basic science classes (1962-1964) and other were brand-new to me. Fetal development of the gland is stimulated by two other hormones released by the hypothalamus and pituitary and those are at high enough levels to cause the fetus to make T4 in clinically significant amounts by 18-20 weeks of gestation. The active hormone, T3, stays at low levels for another 10 gestational weeks, then increases until term.

The net result, it is felt, is protection of fetal development, especially of the brain, in the event the fetus’s mother is herself in a hypothyroid state.

But back to adults and the link between thyroid status and mental health.  One of the crucial measurements of thyroid function is the level of TSH, thyroid stimulating hormone. Normal levels for this pituitary hormone are 0.4 to 5.0 in most labs in the United States; nearly nine years ago, the American Association of Clinical Endocrinologists recommended the doctors consider treating patients whose TSH levels are higher than 3.0. Other scientific groups agreed.

If a TSH level above 5.0 is abnormal, then ~5% of our adult population is hypothyroid. But if that level is reduced to 2.5 to 3.0, then ~20% of us are hypothyroid.

I wonder if a new field of medicine, halfway between the endo folk and the mental health practitioners, is on the horizon.

http://www.umm.edu/endocrin/thygland.htm

Which study should I believe?

Wednesday, October 26th, 2011

Vitamin E has this chemical structure

I just read the recent (Oct 12, 2011) JAMA article on “Vitamin E and the Risk of Prostate Cancer.” It was a long-term, prospective, randomized study of 33,533 men followed in 427 study sites in the US, Canada and Puerto Rico. The investigators were from major academic centers, Duke, the Cleveland Clinic, Brigham and Woman’s Hospital (e.g., Harvard) and the National Cancer Institute among them.

This was an impressive study of the effects of Vitamin E and/or selenium versus placebo that began in 2001 with the subjects being “relatively healthy men.” Seven years after it began, in September 2008, the independent data and safety monitoring committee decided that the supplements should be stopped as there had been no positive results (reduction in prostate cancer detection) and futility analysis (a statistical tool) said the results were quite likely to be negative (more cases of prostate cancer). I hadn’t heard of that term and found a medical website that discussed a number of reasons for ending a study prior to the intended date. I’ll paste in the URL if you want to read a one-pager on what is called “interim analysis.”

http://www.childrensmercy.org/stats/plan/interim.aspx

In this study, though the researchers stopped giving supplements and published an article (JAMA.2009;301(1):39–51) on the results to date, which showed a higher (but not statistically significant) number of cases of  prostate cancer in the groups receiving Vitamin E, selenium or both, they also continued following the patient group.

Prostatic cancer under the microscope

The later data, though July 5, 2011, was quite impressive. There was a 17% higher incidence of prostate cancer in the group taking Vitamin E. In most scientific studies a p-value of 0.05  is felt to be significant. That translates to a probability of 5% or less that whatever happened did so by chance. If the data calculates to a p- value of 0.01, there’s a 1% chance this was a random occurrence. Here, after ~eleven years the p-value for Vitamin E increasing the chance a man was diagnosed with prostate cancer was 0,008. (I’ll paste in a website that explains more of this stuff if you’re remotely interested).   http://www.childrensmercy.org/stats/definitions/pvalue.htm

Why all the math and statistics?

Well, for starters, a few years back a large study showed the exact opposite, but in a highly selected group: men in Finland who were smokers. Another study, done with physicians as the subjects, showed no effect on the incidence of prostate cancer. A post by a physician harshly criticized the SELECT trial as part of a lengthy defense of supplements, but made sweeping pronouncements without supplying data or references to specific articles.

I read the articles, the blog post and the new study in detail. I know that medical research projects often come to conclusions that, a few years later, are “proven” incorrect. But I think this study was carefully done, had a clear-cut purpose in mind and included a large enough group of subjects that I’m going to believe its conclusions.

Plus I’m certainly not a Finnish smoker.