Niacin turbocharges the growth hormone response to anaerobic exercise: A delayed effect

Niacin is also known as vitamin B3, or nicotinic acid. It is an essential vitamin whose deficiency leads to pellagra. In large doses of 1 to 3 g per day it has several effects on blood lipids, including an increase in HDL cholesterol and a marked decreased in fasting triglycerides. Niacin is also a powerful antioxidant.

Among niacin’s other effects, when taken in large doses of 1 to 3 g per day, is an acute elevation in growth hormone secretion. This is a delayed effect, frequently occurring 3 to 5 hours after taking niacin. This effect is independent of exercise.

It is important to note that large doses of 1 to 3 g of niacin are completely unnatural, and cannot be achieved by eating foods rich in niacin. For example, one would have to eat a toxic amount of beef liver (e.g., 15 lbs) to get even close to 1 g of niacin. Beef liver is one of the richest natural sources of niacin.

Unless we find out something completely unexpected about the diet of our Paleolithic ancestors in the future, we can safely assume that they never benefited from the niacin effects discussed in this post.

With that caveat, let us look at yet another study on niacin and its effect on growth hormone. Stokes and colleagues (2008) conducted a study suggesting that, in addition to the above mentioned beneficial effects of niacin, there is another exercise-induced effect: niacin “turbocharges” the growth hormone response to anaerobic exercise. The full reference to the study is at the end of this post. Figure 3, shown below, illustrates the effect and its magnitude. Click on it to enlarge.

The closed diamond symbols represent the treatment group. In it, participants ingested a total of 2 g of niacin in three doses: 1 g ingested at 0 min, 0.5 g at 120 min, and 0.5 g at 240 min. The control group ingested no niacin, and is represented by the open square symbols. (The researchers did not use a placebo in the control group; they justified this decision by noting that the niacin flush nullified the benefits of using a placebo.) The arrows indicate points at which all-out 30-second cycle ergometer sprints occurred.

Ignore the lines showing the serum growth hormone levels in between 120 and 300 min; they were not measured within that period.

As you can see, the peak growth hormone response to the first sprint was almost two times higher in the niacin group. In the second sprint, at 300 min, the rise in growth hormone is about 5 times higher in the niacin group.

We know that growth hormone secretion may rise 300 percent with exercise, without niacin. According to this study, this effect may be “turbocharged” up to a 600 percent rise with niacin within 300 min (5 h) of taking it, and possibly 1,500 percent soon after 300 min passed since taking niacin.

That is, not only does niacin boost growth hormone secretion anytime after it is taken, but one still gets the major niacin increase in growth hormone at around 300 min of taking it (which is about the same, whether you exercise or not). Its secretion level at this point is, by the way, higher than its highest level typically reached during deep sleep.

Let me emphasize that the peak growth hormone level achieved in the second sprint is about the same you would get without exercise, namely a bit more than 20 micrograms per liter, as long as you took niacin (see Quabbe's articles at the end of this post).

Still, if you time your exercise session to about 300 min after taking niacin you may have some extra benefits, because getting that peak growth hormone secretion at the time you are exercising may help boost some of the benefits of exercise.

For example, the excess growth hormone secretion may reduce muscle catabolism and increase muscle anabolism, at the same time, leading to an increase in muscle gain. However, there is evidence that growth hormone-induced muscle gain occurs only when testosterone levels are elevated. This explains why growth hormone levels are usually higher in young women than young men, and yet young women do not put on much muscle in response to exercise.

Reference:

Stokes, K.A., Tyler, C., & Gilbert, K.L. (2008). The growth hormone response to repeated bouts of sprint exercise with and without suppression of lipolysis in men. Journal of Applied Physiology, 104(3), 724-728.

Guest Commentary: Crisis in our Communities - Drug Abuse

Mike Toscani, PharmD
Project Director
Jefferson School of Population Health


I recently attended the American Pain Society Meeting in Baltimore, where I sat in on a symposium on drug abuse facilitated by a principal and students from a recovery high school in Massachusetts. A few key messages rang true, in addition to success stories for individuals with these problems.

The abuse of prescription drugs and illicit substances has risen considerably in the past decade. Strikingly, the use of these substances is increasing in our young population. A recent survey found that almost 10% of 12th graders have experimented with prescription opioids like Vicodin (hydrocodone).

Many cultural and environmental factors have been cited as playing a role in increasing the risk associated with drug abuse, including teens who infrequently eat dinner with their parents, teens who have seen their parents drunk, and parents who do not monitor their teen’s activities and do not safeguard their own prescription medications.

Most teens say that prescription medications are very easy to obtain, and most acquire them from their parents’ or relatives’ medicine cabinets. Some of the recovery high school students spoke in vivid detail of their first experience with alcohol, marijuana or prescription products. Some described that the desire to experience euphoria and the need to continue to use was like a “runaway train” despite the ill feelings, family disputes, threat of law enforcement interventions, and negative social interactions that accompany substance abuse.

Key messages for health professionals include encouraging patients to lock their medicines, dispose of medications when periods of treatment are over (flushing unused medication down the toilet is recommended), and assess and monitor risk in patients who receive controlled substances. Health professionals should take a “universal precautions” approach to those individuals who are prescribed “chronic therapy” with these agents to reduce the potential for abuse. Helpful tools include: risk surveys, opioid treatment agreements, urine drug testing, and reminders to remove medications from areas that can be easily accessed.

New technologies to reduce the risk of tampering and abuse of prescription products are under evaluation by the FDA. Additional data will need to be collected to assess the value of these products in practice.

For more information on drug abuse and attitudes of teens toward drug use, please visit the web sites below:

National Center on Addiction and Substance Abuse at Columbia University

The Partnership for a Drug-Free America. The Partnership Attitude Tracking Study (PATS). Teens 2008 Report. Feb 26, 2009.

Type 4 Series: Formal Style (Rollerset)

This is a series on how to style and manage type 4 hair healthily. It doesn't matter whether you are natural, transitioning, or stretching relaxers.

Today's topic: Roller set type 4 hair with no/low heat. Style into an elegant updo as pictured.

Difficulty level: Easy/Medium for experienced rollersetters or those with short hair, Hard for newbie rollersetters or those with long hair

Time: several hours

Tools: 

moisturizer (no humectants), 

gel (if you're natural; recommend Pantene, Eco Styler),
OR setting lotion (if you're relaxed, transitioning) 

anti-humidity serum (recommend Redken, CHI, Pantene), 

rattail comb, 

ouchless bands, 

snap-on magnetic rollers (size depends on length of hair; the smaller, the longer lasting the style)

OR flexi-rods (more difficult to use)

Instructions:

• Wash, deep condition, detangle as usual
• Apply moisturizer and braid into 6-10 sections with ouchless bands at the roots
• Allow hair to airdry to 70-80% (somewhere between damp + dry but closer to damp).  This step stretches the coils and minimizes the density of natural, shrunken hair.

• One by one, undo each braid, remove the ouchless band, and do the following:
• Part a 1 inch by 2 1/2 inch section of hair
• Apply a moderate amount of gel to the section
• Follow up with a moderate amount of anti-humidity serum 
• Comb with rattail comb and roll tautly with a snap-on magnetic roller
• Repeat until done and move onto the next braid
• After you've finished roller setting, let the hair airdry COMPLETELY. (Alternatively, you may sit under a hooded dryer until hair is dry.)
• Remove the rollers and style as desired.  

[Back in 2008 with flexi-rods]

NOTE:

*It's KEY to let the hair dry completely before removing the rollers.

*The smaller the parts, the tighter and smoother the curls. 

*The smaller the rollers, the tighter and smoother the curls.

*Gel works better on my hair than setting lotion.  Experiment with your hair to see what works for you.

*Reserve this style for dry (non-rainy, non-humid) weather.

Oils, Aloe Vera, and Whipped Hair Butter

It's that time of year again to mix another whipped hair butter!  (My batch ran out this weekend.)  

Ingredients (all are moisturizing):

• unrefined shea butter (softening)
• coconut oil (protection [1] [2])
• olive oil
• safflower OR grapeseed oil (high in fatty acids)
• aloe vera gel
• essential oil (for fragrance, optional)

Instructions:

Read my earlier post on the body butter mixture; the instructions are very similar.  For every cup of shea butter, use 1/4 a cup of olive oil, 1/8 a cup of coconut oil, 1/8 a cup of safflower/grapeseed oil, and a few tablespoons of aloe vera gel.  Of course you can tweak this mixture for a creamier or firmer consistency.  Feel free add drops of your favorite essential oil for fragrance!

FOR THE MIXOLOGISTS:

More whipped butter recipes can be found here.

Hiatus Update

Back from hiatus, but only posting weekly for now.  :)

Growth hormone secretion drops with age, but not exactly in the way you would expect

Many people assume that growth hormone secretion drops with age in a somewhat linear fashion, as implied by this diagram. This assumption probably stems from attempts to model growth hormone variations with linear regression algorithms. This assumption is wrong.

Actual plots of growth hormone secretion patterns, with age on the horizontal axes, tell a different story. See, for example, the graphs below, from professionalmuscle.com. They match the graphs one sees in empirical academic papers. The graphs below (click to enlarge) are particularly good at highlighting some interesting patterns of variation.

On the left side, bar charts show secretion patterns grouped by age ranges during a 24 h period (at the top), during wake time (at the middle), and during sleep (at the bottom). On the right side is the actual data used to build the bar charts. As you can see from the graphs on the right side, the drop in growth hormone secretion follows a pattern that looks a lot more like an exponential decay than a linear pattern.

The drop is very steep from 15 to 40 years of age, after which it shows some fluctuations, going up and down. Interestingly, people in their 50s and 60s, at least in this dataset, have on average higher growth hormone levels than people in their 40s. Of course this may be due to sample bias, but the graphs suggest that there is a major drop in growth hormone secretion, on average, around age 45.

As you can see, there is a lot of individual variation in growth hormone levels. If you look carefully at the graph on the top-right corner, you will see a 50 year old who has a higher 24 h growth hormone secretion than many folks in 15-30 age range. This pattern of individual variation is common for the vast majority of traits anyway, and often the distribution of traits follows a normal, or bell-shaped, distribution. The bell-shaped distribution becomes clear when the traits are plotted based on frequency.

Growth hormone is secreted in pulses. In case you are wondering, growth hormone secretion in young women is higher than in young men. See the graphs below (click to enlarge), from this excellent article on growth hormone by Cummings and Merrian.

Yet, women do not put on a lot of muscle mass in response to weight training, regardless of the age at which they do weight training. This means that growth hormone, by itself, does not lead to significant gains in muscle mass. Androgenic hormones, like testosterone, play a key moderator role here. Muscle mass gain is the result of a number of things, including the combined action of various hormones. To complicate things further, not only do these hormones act together in an additive fashion, but they also influence each other.

Another reasonable conclusion from the data above on growth hormone secretion in young women and men is that growth hormone must indeed have major health-promoting effects, as most of the empirical data suggests. The reason is that, from an evolutionary standpoint, young (or pre-menopausal) women have always been the evolutionary bottleneck of any population of ancestral hominids. High survival rates among young women were a lot more important than high survival rates among men in general, in terms of the chances of survival of any population of ancestral hominids.

Higher survival rates among young ancestral women may have been enabled by higher levels of growth hormone, among other things. The onset of the metabolic syndrome, which is frequently in modern humans around age 45, may also be strongly influenced by falling growth hormone levels.

How can growth hormone secretion be increased after age 45? One obvious option is vigorous exercise, particularly resistance exercise.

Cortisol response to stress is much more elevated with ingestion of glucose than with protein or fat

Cortisol is a hormone that does a number of different things; a jack of all trades among hormones, so to speak. It tells the liver to produce glucose, preventing hypoglycemia. It also tells the liver to synthesize glycogen, which is in some ways the opposite of producing glucose. It tells the stomach to secret gastric acid. It is an anti-diuretic hormone. It suppresses the immune system, which is why it is frequently used to reduce inflammation, and treat allergies and various autoimmune diseases. It jump-starts an increase in free fatty acids in circulation, thus helping provide an important source of energy for endurance exercise.

Cortisol, together with epinephrine (a.k.a. adrenaline), even contributes to the creation of surprise-induced memories. It is because of this action of cortisol that Americans reading this post, especially those who lived in the East Coast in 2001, remember vividly where they were, what they were doing, and who they were with, when they first heard about the September 11, 2001 Attacks. I was living in Philadelphia at the time, and I remember those details very vividly, even though the Attacks happened almost 10 years ago. That is one of the fascinating things that cortisol does; it instantaneously turns short-term contextual memories temporally associated with a surprise event (i.e., a few minutes before and after the event) into long-term memories.

Similarly to insulin, you don’t want cortisol levels to be more elevated than they should naturally be. Natural levels being those experienced by our hominid ancestors on a regular basis. You need cortisol, but you don’t need too much of it. Many tissues in the body become resistant to hormones that are more elevated than they should be, like insulin and leptin, and this is also true for cortisol. It is a bit like people constantly shouting in your ears; after a while you cover your ears, or they get damaged, so people have to shout louder. If you frequently have acute elevations of cortisol levels, they may become chronically elevated due to cortisol resistance.

Chronically elevated cortisol levels are associated with the metabolic syndrome, the hallmark of the degenerative diseases of civilization.

Stress causes elevated cortisol levels. And those levels are significantly elevated if you consume foods that lead to a high blood glucose response after a meal. That is what an interesting experimental study by Gonzalez-Bono and colleagues (2002) suggests. The full reference and link to the study are at the end of this post. They used glucose, but we can reasonably conclude based on glucose metabolism research that foods rich in refined carbohydrates and sugars would have a very similar effect. If we think about the typical American breakfast, possibly even a stronger effect.

In order to do their study they needed to put the participants under stress. To cause stress the researchers did what many college professors have their students do at the end of the semester, which is also something that trial lawyers and preachers are good at, and something that most people hate doing. You guessed it. The researchers had their subjects do, essentially, some public speaking. The experimental task they used was a variation of the “Trier Social Stress Test” (TSST). The researchers asked the participants to conduct a 5-minute speech task and a 5-minute mental arithmetic task in front of an audience.

The participants were 37 healthy men who fasted for at least 8 h prior to the study. They were randomly assigned to one of four groups. The glucose group consumed 75 g of glucose dissolved in water. The fat group consumed 200 g of avocado. The protein group drank 83 g of proteins dissolved in water. The fourth group, the water group, drank plain water.

From a real world perspective, the fat and protein groups, unlike the glucose group, were arguably overloaded with their respective nutrients. Many people would not normally consume that much fat or protein in one single meal. This makes the results even more interesting, because it seems that fat and protein lead to virtually the same response as water, regardless of the amount ingested. The table below shows the cortisol responses for all groups.

As you can see, the cortisol response for the glucose group is a lot more elevated. How much more elevated? In the inner square at the top-left part of the figure you have the areas under the curve (AUC), which are essentially the estimates of the integrals of the cortisol curves for each of the groups. Usually AUC is a key measure when one looks at the potential negative impact of the elevated levels of a substance in the blood. Note that the cortisol AUC for the glucose group is much larger, about two times larger, than the cortisol AUCs for the other groups.

When one has a morning car commute, what is going to happen? Typically cortisol levels will be elevated, unless the commute is uneventful and done completely on “automatic pilot”; which is not very common, as people cut off in front of each other, make irritating mistakes etc.

What if, before that commute, one eats a “solid” breakfast with plenty of “healthy” sugary cereal covered with honey, a glass of “healthy” low-fat milk (of course, because fat “raises bad cholesterol”), and maybe three pancakes covered with syrup?

Cortisol levels will be much more elevated.

Doing this often, maybe after several years a person will become eligible for death by sudden cardiac arrest while doing some light activity.

Reference:

Gonzalez-Bono, E., Rohleder, N., Hellhammer, D.H., Salvador, A., & Kirschbaum, C. (2002). Glucose but Not Protein or Fat Load Amplifies the Cortisol Response to Psychosocial Stress. Hormones and Behavior, 41(3), 328–333.