Resistant Starch Experiment

I have read a lot about the benefits of resistant starch over the past few years.  I highly recommend you read posts on the subject by Mark Sisson and Chris Kresser to learn more about this form of starch.

I settled on Bob's Red Mill Potato Starch for my experiment.  This is classified as an RS2 form of starch.

I started out by consuming one teaspoon per day, taken about an hour before dinner.  I built up slowly to one tablespoon per day, which I continued for two months.  I should note that I did not take a probiotic during this time period, which might have been a mistake.

I did not notice any benefits, but did experience a decrease in gut health  (use your imagination).  This may be due to not taking a good probiotic during these two months.

I am now loading up on probiotics in hopes that I can make my gut happy again. I am rotating through Garden of Life Primal Defense Ultra, Prescript Assist and AOR ProBiotic 3.

I am unsure if I will try this experiment again with a probiotic.  I have read more posts on why RS2 might not be a good idea and is perhaps no more than hype.  A case in point is the lengthy blog post by Dr. BG.

Now to ponder the next big experiment.

Enjoy!


[UPDATE: January 9, 2015] - I have successfully re-seeded my gut using a combination of Mt. Capra Caprobiotics Advanced, Mt. Capra Capracolostrum, Prescript Assist, and AOR ProBiotic 3. I do not plan on re-starting resistant starch again any time soon.

How exercise changes your genes

The below is a great article on new findings relative to how exercise effects the expression of some of your genes.  This is one example of how lifestyle choices effect your health (Epigenetics).  Others include diet, sleep/recovery, and stress.

http://well.blogs.nytimes.com/2014/12/17/how-exercise-changes-our-dna

CreditGetty Images

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PHYS ED

Gretchen Reynolds on the science of fitness.

We all know that exercise can make us fitter and reduce our risk for illnesses such as diabetes and heart disease. But just how, from start to finish, a run or a bike ride might translate into a healthier life has remained baffling.

Now new research reports that the answer may lie, in part, in our DNA. Exercise, a new study finds, changes the shape and functioning of our genes, an important stop on the way to improved health and fitness.

The human genome is astonishingly complex and dynamic, with genes constantly turning on or off, depending on what biochemical signals they receive from the body. When genes are turned on, they express proteins that prompt physiological responses elsewhere in the body. 

Scientists know that certain genes become active or quieter as a result of exercise. But they hadn’t understood how those genes know how to respond to exercise. 

Enter epigenetics, a process by which the operation of genes is changed, but not the DNA itself. Epigenetic changes occur on the outside of the gene, mainly through a process called methylation. In methylation, clusters of atoms, called methyl groups, attach to the outside of a gene like microscopic mollusks and make the gene more or less able to receive and respond to biochemical signals from the body. 

Scientists know that methylation patterns change in response to lifestyle. Eating certain diets or being exposed to pollutants, for instance, can change methylation patterns on some of the genes in our DNA and affect what proteins those genes express. Depending on which genes are involved, it may also affect our health and risk for disease.

Far less has been known about exercise and methylation. A few small studies have found that a single bout of exercise leads to immediate changes in the methylation patterns of certain genes in muscle cells. But whether longer-term, regular physical training affects methylation, or how it does, has been unclear.

So for a study published this month in Epigenetics, scientists at the Karolinska Institute in Stockholm recruited 23 young and healthy men and women, brought them to the lab for a series of physical performance and medical tests, including a muscle biopsy, and then asked them to exercise half of their lower bodies for three months. 

One of the obstacles in the past to precisely studying epigenetic changes has been that so many aspects of our lives affect our methylation patterns, making it difficult to isolate the effects of exercise from those of diet or other behaviors.

The Karolinska scientists overturned that obstacle by the simple expedient of having their volunteers bicycle using only one leg, leaving the other unexercised. In effect, each person became his or her own control group. Both legs would undergo methylation patterns influenced by his or her entire life; but only the pedaling leg would show changes related to exercise.

The volunteers pedaled one-legged at a moderate pace for 45 minutes, four times per week for three months. Then the scientists repeated the muscle biopsies and other tests with each volunteer.

Not surprisingly, the volunteers’ exercised leg was more powerful now than the other, showing that the exercise had resulted in physical improvements.

But the changes within the muscle cells’ DNA were more intriguing. Using sophisticated genomic analysis, the researchers determined that more than 5,000 sites on the genome of muscle cells from the exercised leg now featured new methylation patterns. Some showed more methyl groups; some fewer. But the changes were significant and not found in the unexercised leg.

Interestingly, many of the methylation changes were on portions of the genome known as enhancers that can amplify the expression of proteins by genes. And gene expression was noticeably increased or changed in thousands of the muscle-cell genes that the researchers studied.

Most of the genes in question are known to play a role in energy metabolism, insulin response and inflammation within muscles. In other words, they affect how healthy and fit our muscles — and bodies — become.

They were not changed in the unexercised leg.

The upshot is that scientists now better understand one more step in the complicated, multifaceted processes that make exercise so good for us.

Many mysteries still remain, though, said Malene Lindholm, a graduate student at the Karolinska Institute, who led the study. It’s unknown, for example, whether the genetic changes she and her colleagues observed would linger if someone quits exercising and how different amounts or different types of exercise might affect methylation patterns and gene expression. She and her colleagues hope to examine those questions in future studies.

But the message of this study is unambiguous. “Through endurance training — a lifestyle change that is easily available for most people and doesn’t cost much money,” Ms. Lindholm said, “we can induce changes that affect how we use our genes and, through that, get healthier and more functional muscles that ultimately improve our quality of life.” 

"I want to Run a 7-Minute Mile When I'm 130" - Q&A with Bill Andrews, the ultrarunning geneticist who wants to cure aging

I first heard about Bill Andrews when he was on one of Dave Asprey's first podcasts.  Bill is trying to find the right combination of nutrients which will either stall the shortening of one's telomeres or perhaps even allow them to grow back. The first two products which purport to do this, but have a very minor impact are, TA-65 and Isagenix Product B.

Below is the interview Trail Runner conducted with Bill.

http://trailrunnermag.com/people/q-and-a/article/1588-bill-andrews-ultrarunning-geneticist-curing-aging

Bill Andrews, a geneticist working to halt human aging, often jokes that he’s going to “live forever ... or die trying.”

If it seems odd that a serious scientist with a Ph.D. in Genetics from the University of Georgia would make light of his own research by quoting comedian Groucho Marx, well, Andrews is not your typical lab rat.

The 63-year-old president and CEO of Reno, Nevada, biotech firm Sierra Sciences is an avid ultramarathoner who’s run some of the country’s hardest ultras, including the Leadville Trail 100, the Western States 100 Mile Endurance Run and the Badwater Ultramarathon.

"I was always a runner," says Andrews, who is married to fellow ultrarunnerMolly Sheridan. "When I was a little kid, I ran everywhere. I was just fortunate enough to have parents who didn’t tell me all the time to quit running."

Andrews ran cross country and track in high school and college and marathons during graduate school, then got into ultramarathons in his 30s, running his first 50-miler in 1996.

"I had such fun that I signed up for another 50-mile run a week later," he says. He ended up running some 20 50-mile races that year.

When he's not running, Andrews can be found in his lab, working on what he calls a "cure for aging." His research focuses on telomeres, the tips of our chromosomes, which shorten every time our cells divide. That shortening is one of the root causes of human aging and the diseases that come with it. Andrews' work on telomeres is the subject of a new documentary, The Immortalists.

Trail Runner caught up with Bill to talk about his research on aging and why ultrarunners are biologically younger than everyone else.

When you say “curing aging,” what exactly do you mean?

I do get criticized occasionally for using the term “curing aging,” because a lot of people say aging is normal: it’s not a disease and therefore you can’t cure it. But we’ve known for a long time that we do have this theoretical maximum lifespan of 125 years, extrapolated from looking at populations since the Roman days—with no explanation as to what’s going on. Of course, when you’re close to 125, you’re very, very unhealthy.

No one in documented history has ever lived to be 125. The closest is 122. Now, I say that when a person exceeds 125 and is still healthy enough that they can do things that a young person can do, aging’s been cured.

I frequently say that I’m going to run a 7-minute mile when I’m 130 years old. [If I succeed], everyone’s going to jump on board and say, “Aging’s cured," not just me.

What inspired you to work on human aging?

As a young boy, I was fascinated by all the things that might happen in the future, including the discovery of life on other planets and all the things we were going to learn from it. I wanted to be around when all that happened. And my father pointed out to me, “You know, that that’s probably not going to happen in your lifetime—unless you go out and find a cure for aging.”

I turned my attention on curing aging in the early 1990s, when I attended a seminar where somebody talked about the fact that telomeres get shorter as you age and are much better at telling a person how old they are than reading the palm of their hand.

How do telomeres work?

Telomeres are the very tips of our chromosomes. When the caps on our shoelaces get shorter, our shoelaces start to fall apart, and the same thing happens to our chromosomes. When our telomeres get short, our chromosomes start falling apart, and that results in much of the decline of health when we grow older.

[Telomere shortening] is generally correlated with chronological age, but it’s more of a measure of biological age and health. So you can get telomere shortening when you’re young, and that ends up giving you age-related diseases.

Every single time our cells divide, our telomeres get a little bit shorter. But this can’t be true in all of our cells, because we’re all a product of cell division from one generation to the next. If it were true in all of our cells, our children would be born with shorter telomeres than we have, but that’s not the case. We discovered an enzyme called telomerase that’s found in our reproductive cells and actually keeps the telomeres from shortening. Every time a [reproductive] cell divides, the telomere gets a little bit shorter. But then telomerase re-lengthens it.

It turns out there are life forms on this planet that have no detectable aging process. Lobsters, humpback whales, clams, some fish, some birds, tortoises—all these animals have no detectable aging process. 150 years later, those animals are still healthy, moving around like young animals. All these animals have been shown to produce telomerase in all their cells already. We only produce it in our reproductive cells. I want to make it so it will be in all our cells.

Is there a connection between running and biological age?

Molly and I have both noticed that a lot of people in the sport of ultramarathon running look young and act young. There are 80-year-olds who are very competitive. When I ran my very first 100-mile race, my mentor, Helen Klein, was 75 at the time, running a 100-mile race. She stayed with me for the first 95 miles of the race, teaching me the ropes, then said, “Well, Bill, I think you’ll make it to the finish line now.” And after 95 miles she took off ahead. So something’s going right there. And now there’s science actually supporting that.

Have you yourself done any scientific work on running and aging?

No, my focus is pretty much on looking at human cells in a petri dish. But I do keep up with the scientific literature, and a lot of papers have shown the opposite viewpoint of what it used to be. Endurance exercise is only looking like a good thing.

How so?

A sedentary lifestyle is a good way to increase the rate of your telomere shortening, accelerating your aging and decline in health. Studies in peer-reviewed scientific journals have shown that one of the best things you can do to extend your lifespan and health span is intense endurance exercise—and by "intense" I mean how far you go, and how often you go that far, not how fast you go. People who are sedentary have shorter telomeres than people that run 10K races. 10K racers have shorter telomeres than people who run marathons. And people who run marathons have shorter telomeres than people who run ultramarathons.

So ultramarathon runners are looking like the people who have the longest telomeres—and it’s well established now that the length of your telomeres is a very good indicator of your overall health and aging.

What we’ve found (and when I say we, I mean other scientists) is that when humans exercise consistently—at least, endurance exercise, and it can be bicycling, swimming, it doesn’t have to be just running—their antioxidant levels increase so much more than their free radicals [which also increase with exercise] that their net oxidative stress is actually less.

It’s been shown that if you have high oxidative stress [such as from obesity or smoking], the free radicals will cleave your telomeres and cause what I call “accelerated telomere shortening.” That causes accelerated aging and decline of health.

All kinds of things have been shown to decrease the rate of accelerated telomere shortening. Endurance exercise is the number-one best thing you can do. Losing weight is also important. Quitting smoking is really, really important. Reduce stress. Be optimistic: studies have shown that people who don’t believe they’ll live to 100 actually won’t, because their telomeres are shorter, though nobody has an explanation as to why that’s the case. You can also take supplements : Vitamin D, Omega-3 fatty acids, antioxidants, Vitamin E. Doing these things will increase your chances of living to 125.

By the way, I mentioned that nobody knew why we had this theoretical maximum lifespan of 125 years. But now the mathematics of telomere shortening explain it perfectly. Even the healthiest person who has zeroaccelerated telomere shortening will have enough telomere shortening just from cell division (what I call basal level telomere shortening) that they’ll still only have a maximum lifespan of 125.

Is there anything that actually lengthens telomeres?

There’s shortening and lengthening going on at the same time. It’s like a tug-of-war. But there’s nothing that’s been discovered, except for gene-therapy techniques, that will have a net result of overall telomere lengthening. But that’s something I think I will have by mid-2016.

Have you faced any criticism for your work on aging?

The problem is that quacks and charlatans have been discrediting the field of anti-aging for thousands of years. Even with all the great science, people are still skeptical and don’t believe it’s real. After starting my company in 1999, my investors wanted us to be kept totally under the radar. Nobody even knew we existed. We started off leasing lab space from a university, and even the other scientists in the same hallway as us, working on unrelated projects, never knew what we were doing. We had a fictitious story that we were doing something else.

But in the last five years, that has really turned around. [At screenings of The Immortalists] doing Q&A afterwards, I would be there for three hours answering questions. People are super fascinated by the idea that we’re actually on the verge of curing aging.

There would be some people who actually argue that this is wrong, because it’ll cause overpopulation and young people are never going to be able to compete for jobs if people don’t get old and retire. They’re right, all these problems are going to occur. But nobody [now] says, “Oh, this is a bunch of quackery.” The only question now is: Is this a good thing or a bad thing to do?

I assume your answer is "a good thing."

I’m open to saying, “Yes, I’m going to create havoc all over the world by curing aging. Please, somebody else, figure out how to solve it.”

But I believe that the future problems are going to be a lot more tolerable than the present ones. People don’t realize how many old people there are, unable to take care of themselves, having caregivers have to do everything for them. The problem’s just getting worse. We’re on the verge of what’s called a “silver tsunami”: by 2020 we’re going to have so many old people in the world it’s going to be the number one industry. I tell high-schoolers, “If you’re looking for a career that’s gonna have a lot of job openings, it’s care for the elderly.”

If I can cure aging, the world won’t have that problem. People will stay young and not get unhealthy, at least not at the rate that they are now.

One of the PR taglines for The Immortalists is, “Bill Andrews wants to cure aging ... or die trying.” I have to ask, is that a PR conceit or your actual motto?

Back in 2005, I was giving a presentation to a group of investors. This was still when we were under the radar. After I finished, a skeptic in the back said, “So you really think you’re gonna cure aging?”

I just replied, very seriously, “You know, or die trying.”

Everybody started laughing. That ended up becoming our company motto. We have signs on the walls saying, “Cure aging or die trying.” When we started letting people like Popular Science into the building to interview us and take pictures, they really latched onto that. They made it into a PR pitch.

But it’s still something I believe in. I just hope I don’t end up “dying trying.”

Strength and Conditioning Research Interview: Andrew Flatt on HRV

http://www.strengthandconditioningresearch.com/2014/11/18/andrew-flatt-hrv/

The below interview provides a great background on Heart Rate Variability (HRV) and how it can be used to optimize training and recovery.

Chris Beardsley (@SandCResearch) interviews Andrew Flatt (@andrew_flatt), a researcher working on Heart Rate Variability (HRV) at the University of Alabama.

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Chris: Thanks for the interview, Andrew, we really appreciate your time. Can you tell us, what exactly are we measuring when we record HRV? What are the main measurements? Do each of these measurements of HRV tell us different things?

Andrew: My pleasure, Chris. This site has been a tremendous resource for me since day one and I am happy to contribute to the great content you provide.

In order to assess heart rate variability (HRV), a recording of beat to beat or “R-R” intervals is required. Subtle changes in heart rate regularly occur in response to respiration where HR tends to speed up during inspiration and slow down during expiration. With various mathematical and statistical procedures, we can quantify and assess heart rate variability.

The human heart is equipped with an intrinsic pacemaker called the sinoatrial (SA) node that when left alone sets heart rate at approximately 75 beats per minute, give or take. However, a component of our central nervous system called the autonomic nervous system largely influences SA node activity and thus heart rate.

Parasympathetic and sympathetic nerves extend from the brain stem and directly innervate the heart. Parasympathetic stimulation (via the vagus nerves) tends to inhibit SA node activity via the release of acetylcholine and therefore reduces heart rate and increases variability. Sympathetic stimulation has the opposite effect where SA node activity is increased via the release of norepinephrine which will speed up heart rate and reduce variability.

Therefore, assessing HRV provides a non-invasive measure of centrally mediated cardiovascular-autonomic control. Though numerous HRV parameters exist, the most commonly assessed for athlete monitoring include:

• The log transformed root mean square of successive R-R interval differences (lnRMSSD),
• High frequency spectral power (HF)
• Low frequency spectral power (LF)
• The LF to HF ratio (LF:HF)

LnRMSSD and HF are both representative of parasympathetic activity and tend to correlate quite well with each other. What LF reflects is less clear. It was initially thought that LF reflects sympathetic activity and thus LF:HF provides a nice indication of the balance between sympathetic (LF) and parasympathetic (HF) activity. However, this doesn’t appear to be the case. LF is influenced by both parasympathetic and sympathetic activity and particularly by the baroreflex, which functions to help regulate blood pressure. Therefore, what exactly the LF and LF:HF means is not entirely clear.

For athlete monitoring purposes, parasympathetic activity, assessed via RMSSD or HF, is of primary interest for assessing recovery status and physiological adaptation to training.

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Chris: That’s an amazingly comprehensive introduction to HRV, Andrew, thank you. Many reviewers of HRV have recommended using 5 – 10 minutes of resting time for accurate measurements. Do you think shorter measurement durations of HRV can be performed and still tell us something?

Andrew: The topic of HRV recording methodology, specifically as it pertains to measurement duration, has been an area that my colleague Dr. Michael Esco and I have been investigating. Standardized guidelines recommend that a recording period of 5 minutes preceded by a 5-minute stabilization period be used to establish short-term HRV.

These guidelines were primarily developed for clinical/laboratory purposes and assume that a variety of HRV indexes will be included for analysis as some indexes require several minutes for determination (e.g, LF). This may not be a big issue if HRV was assessed only periodically. However, it’s quite clear that daily HRV measures are preferred over weekly, or less frequent measures to be meaningful for athletes. It would therefore be unreasonable for coaches to expect athletes to spend 10 minutes each morning performing an HRV measurement. In light of this, we wanted to determine: a) how short of an HRV recording we get away with that is still valid, and b) how long it takes HRV to stabilize before we should start recording a measure.

To try and answer some of these questions we directed our focus on lnRMSSD. lnRMSSD has been suggested to be the preferred HRV index for athlete monitoring for a variety of reasons. Compared to HF, lnRMSSD is less influenced by breathing rate and provides a lower coefficient of variation across measures, thus making it a more reliable marker. Remember that we have to rely on our athletes to take proper HRV recordings for the data to be useful, so eliminating potential issues such as breathing rate may be helpful.

Since lnRMSSD is a statistical measure, it can be easily calculated in Excel if the R-R interval data is available. In addition, the lnRMSSD is easily interpretable for the end user, particularly when it is modified on a ~100 point scale (done in popular smart phone apps) by simply multiplying the lnRMSSD value by 20. Therefore, when individuals are performing self-measures of HRV at home with a field tool (e.g., smart phone application), the lnRMSSD appears to be the most practical and appropriate.

Our research indicates that lnRMSSD can be accurately assessed in athletes in only 60-seconds and that lnRMSSD stabilization appears to occur within about one minute. This research was done with collegiate athletes and involved ECG measures in the supine position. We are continuing to explore this area with a fellow colleague, Dr. Fabio Nakamura where we are assessing the agreement between 60-second lnRMSSD measures with traditional 5-minute recordings in addition to the time-course for lnRMSSD stabilization.

This work in collaboration with Dr. Nakamura involves elite team sport athletes who self-recorded HRV with a field tool in the seated position. This is an important next step because field tools require less subject preparation for HRV measurement compared to ECG and the seated position may be preferred over supine measures, particularly in highly fit individuals. Based on our recent findings and preliminary analysis from our more current project, I am confident that meaningful HRV data can be collected in much shorter than 10 minutes.

In a recent case study,  we monitored HRV with a smart phone app using a 55-second HRV recording after waking in a seated position in a collegiate endurance athlete. We found that the weekly CV correlated almost perfectly with weekly 8 km race times.

In another case study currently being written up, we found that weekly mean HRV related well to training load during competition preparation in a high level powerlifter with cerebral palsy. HRV was recorded with the same app under the same conditions (i.e., waking, seated). Taken with all of the other data I’ve collected on myself and other athletes I’ve worked with, I’m quite confident that meaningful HRV data can be collected with ultra-short measures and minimal stabilization periods for lnRMSSD.

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Chris: Great insights into HRV, again, thank you Andrew. Interpretation of HRV measurements seems very complex. Do you have any general rules of thumb for what HRV metrics to measure and what different movements mean?

Andrew: The problem with providing general guidelines for HRV interpretation is that this would assume a homogenous group of individuals who do not differ by training level (elite, amateur), age, fitness level, race, gender, sport, exercise modality (resistance training, intervals, steady state) and so forth. HRV responses are largely individual which increases the complexity of interpretation, but at the same time, provides a unique physiological marker to consider when assessing training status and responses.

Some very important review papers on this topic (see references) have been written by researchers who are both athletes and coaches. I would encourage people to read these. Based on the available research and my own experimentation, there are 3 main values that I use for HRV (all of which use lnRMSSD) interpretation with athletes:

1. Acute or daily HRV change
2. Weekly mean HRV change
3. Weekly coefficient of variation (CV) change

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#1. Acute changes

Once a baseline is established (a one-week mean works well for this), it is easy to determine when a daily change is well above or below baseline. Intense training sessions or novel training stimuli (new exercises, set/rep schemes, conditioning, etc.) will generally result in an acute decrease in HRV that can take between 48-72 hours to return to baseline.

Over the course of a training cycle, acute changes will generally become smaller (smaller decrease in HRV, faster return to baseline), which I interpret to mean positive adaptation to the training (more on this below with discussion of CV).

Moderate aerobic exercise tends to have a stimulatory effect on parasympathetic activity and therefore it is common to see increases in HRV 24 hours after this type of exercise and thus has been suggested as an effective active recovery tool.

It’s important to understand however that HRV is sensitive to a wide variety of physical, chemical and psychological stimuli, and therefore an acute HRV measure can be obscured by non-training related stressors. For example, alcohol, poor sleep, nutrition, pharmaceuticals and so forth can all impact HRV.

Therefore, though the acute changes in HRV are meaningful, I would suggest that coaches use caution when trying to determine training prescription solely based on an acute change. Another prime example of this is the anxiety/excitement experienced by athletes on the day of competition which often results in a low HRV score. This certainly does not mean however that they are fatigued or not prepared to perform. Context is very important when interpreting acute changes.

HRV has primarily been researched in endurance athletes. Adjusting training on a daily basis according HRV changes is likely most effective in that population. There has yet to be any research that evaluates HRV guided training for strength/power athletes. An acute increase or decrease in HRV likely will not differentiate strength power/performance except for in obvious situations, like when HRV is low due to heavy drinking the night before, or because of very intense training. In this case, the low HRV score will likely relate to reduced performance.

HRV may still be useful for strength/power athletes, though serving more as a global marker. For example, during overload weeks (high volume resistance training) there will definitely be some HRV changes compared to lower load weeks. The question really is whether HRV data provides any additional useful information that other training load and performance data does not provide. This is an area my colleague and I will explore in the future.

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#2. Weekly mean changes

The weekly mean provides the coach with a simple value that may provide a good indication of the weekly load experienced by the athlete. An increase in the weekly mean for the most part is reflective of positive adaptation or quality recovery.

In some cases however, increases in the weekly mean can be indicative of high fatigue, although this is generally in response to very high volumes of endurance training. Taken into context of the weekly training load and other markers of training status (e.g., wellness, performance), it should be easy to determine if the mean HRV change indicates positive or maladaptive responses.

The weekly mean is influenced by the content of aerobic exercise performed in that week. Moderate to high levels of aerobic work will generally increase mean values (up to a point) since this type of work has that stimulatory effect on parasympathetic activity. Therefore, decreases in a weekly mean value may be reflective of reductions in aerobic activity. Higher intensity exercise can result in greater acute HRV responses decreases and thus effect the weekly mean. Therefore, coaches should use caution when trying to asses fitness based on weekly mean HRV. Again, context is key.

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#3. Weekly CV changes

The CV reflects the variance in HRV scores across the week that is not captured in the weekly mean value. The CV is easily calculated as the standard deviation divided by the mean and expressed as a percentage. Higher CV values indicate higher variance in scores across the week, and lower CV values indicate less variation in scores across the week.

High variation in day to day scores may indicate the fatigue (low scores) and recovery (return to or above baseline) process from a week of training. A higher CV likely reflects a higher training load, or a more stressful week (perhaps due to travel schedules, etc.).

In my experience, a gradual reduction in the CV throughout training is indicative of positive adaptation. In our case study of the collegiate runner, lower CV values were almost perfectly related to his 8km run times, where his worst performances occurred on weeks with the higher CV and his best performances occurred on the weeks with the lowest CV.

In a female collegiate soccer team, we are seeing that CV changes are relating to training load and performance changes. It should be noted that a reduced CV was related to the development of overtraining in an elite female triathlete in a case comparison study by Daniel Plews and colleagues. Therefore, as with each of the other values, the CV must be taken into context.

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Chris: That’s a really helpful how-to guide for HRV measurements, thank you Andrew. Is there any other practical guidance would you offer a coach who was looking to start implementing monitoring HRV measurements with a team of athletes?

Andrew: Here are some final suggestions to coaches who are interested in using HRV with their athletes.

Experiment with a handful of athletes before you try and attempt to implement HRV monitoring with an entire team. This will be much more manageable in terms of data collection and analysis. Consider this a trial run to determine if HRV will be practical in your situation. This includes assessing a) if you think your athletes can reliably perform self-measures at home, and b) if the data you are collecting is actually meaningful.

Don’t start using HRV if you currently do not monitor any other training status markers. For one, HRV is much less meaningful when taken alone. It would be difficult to put an HRV score into context if you do not know what training load (sRPE, tonnage, distance, etc.) was or how wellness scores are evolving. Start with the basics first.

When assessing team HRV data, use the team mean to assess the general responses of the team as a whole. But understand that it is the individual responses that are more important. Some athletes will be responding favorably while others will not. HRV can be useful for helping determine which athletes fall into which category and thus may influence decision making for intervention.

Although smartphone apps conveniently display a nice visual of the HRV trend, you will likely need to also perform some further analysis in Excel, specifically for assessing mean and CV. Most apps have an “export” function that allows you to download a spreadsheet of the data. Specific statistical procedures for determining meaningful changes in HRV from such downloaded data can be found in Martin Buchheit’s paper (see references).

Also, if you want to compare your data from a smartphone download to published lnRMSSD values, you will need to divide your score by 20 (if using the ithlete or BioForce apps). For example, An HRV score of 83 with ithlete or Bioforce is actually an lnRMSSD value of 4.15 (83/20 = 4.15). These values are multiplied by 20 in the smartphone apps to transform the lnRMSSD value to fit onto an approximately 100-point scale for more intuitive interpretation by the casual end user. Also, be sure to note what position HRV is measured in when comparing to published data as supine values will be different than seated or standing values.

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Chris: Thanks for your time, Andrew!

If you are interested in learning more about HRV and would like to contact or follow Andrew Flatt, please follow him on Twitter or check out his blog.

If you would like to do graduate work exploring HRV, the University of Alabama has a dedicated laboratory with the latest equipment, making it the place to go. Contact Andrew on hrvtraining(at)gmail.com for more details.

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References

1. Buchheit M. Monitoring training status with HR measures: do all roads lead to Rome? Front Physiol (2014); 5.
2. Plews DJ, Laursen PB, Stanley J, Kilding AE, Buchheit M. Training adaptation and heart rate variability in elite endurance athletes: Opening the door to effective monitoring. Sports Med (2013); 43; 773-781.
3. Stanley, J., Peake, J. M., & Buchheit, M. Cardiac parasympathetic reactivation following exercise: implications for training prescription. Sports Med, 43:1259-1277, 2013.

Magnesium - The often overlooked micronutrient

I have augmented my diet with magnesium supplements for several years.  I, like many people, believed I was getting ample amounts of magnesium from my diet.  Despite this, I noticed I was experiencing more cramps in my legs the morning after hard training runs or races as I got older.  I had recalled reading about the importance of magnesium for numerous biochemical functions and that you deplete your magnesium through exercise.

Katy and I started out drinking Natural Calm every evening before retiring to bed.  Low and behold, both of us stopped experiencing cramping almost immediately.

We have since augmented the Natural Calm with Natural Stacks Magtech, which is a broader spectrum source of magnesium, including L-Threonate, which aids cognitive function and memory.

Below are two great videos by Dr. Rhonda Patrick concerning the role magnesium plays in health.  I encourage you to watch these videos and to go to http://www.foundmyfitness.com to check out her other great content.

Krill Oils DHA - Brain Advantage

The below article on Fish versus Krill oil was written by Dr. Rhonda Patrick.  Dr. Patrick is one of my favorite research junkies whose work I follow closely.  As for my daily omega-3 intake, I alternate between Barlean's Wild & Whole Alaskan Salmon Oil and Nordic Naturals Ultimate Omega in the morning, and Natural Stacks Anarctic Krill Oil in the evening. I hope you enjoy the below article and encourage you to sponsor Dr. Patrick so she can continue to produce her well researched content. There has been a lot of health experts recently advocating strongly for krill oil as an allegedly superior alternative to fish oil as a source for omega-3s. Today we are going to get into the nitty gritty of fish and krill oil and hopefully shed some light on their similarities as well as differences, which may lead to benefits that are actually specific to different tissues in the body. It's undeniable that the essential omega-3 fatty acids, particularly eicosapentaenoic acid (known as EPA) and docosahexaenoic acid (known as DHA) are extremely important in human physiology. In fact, because fish oil is already one of my single favorite supplements, it's pretty hard for me to even entertain the notion that there's any room for some sort of trade-up from the awesomeness of fish oil. There may be some truth to it, however, within certain very specific contexts. Omega-3 (EPA & DHA) are essential fatty acids and are required by the human body. They cannot be synthesized by our bodies and must be obtained from the diet. One study using data from the National Center for Health Statistics looked into the most common dietary, lifestyle, or metabolic risk factors influencing early mortality found that low intake of omega-3 fatty acids was one of the top dietary factors that had the largest influence on mortality and it accounted for around 80,000 to 100,000 deaths in 2005 alone. [1] The "Benefits" of Omega-3 But... before we dive into krill oil and a comparison between it and fish oil, let's briefly go over just a few of the established benefits of EPA and DHA that are generalizable: Supplementation with EPA and DHA omega-3 fatty acids has been shown to: Lower all-cause mortality. Prevent telomere shortening (the biological measure of aging) (read more.) Improve learning and memory. Delay brain aging by repairing damage and preventing atrophy. Reduce inflammation, immune system hyperactivity that damages tissues and can also initiate cancer Positively affect cholesterol profile by increasing HDL and lowering triglycerides. Increase cell membrane fluidity including in neurons, which is critical for the action of neurotransmitters including norepinephrine, which has been shown to play a very important role in focus and attention. On the topic of cell membrane fluidity and norepinephrine, it plays a very important role in many, many different cellular functions. However, just to make it a little bit more tangible one particular example worth mentioning is the fact that DHA is necessary for the adrenergic receptor (found in the cell membrane) to be able to bind to norepinephrine so that norepinephrine can induce a biological response in the brain. Norepinephrine in particular has been shown to play a very important role in focus and attention. See my video on hyperthermic conditioning to learn more about norepinephrine in the context of sauna use. Neurotransmission, however, isn't the only place where membrane fluidity is critical. In fact, many other cell types also have proteins (like receptors) bound to the membrane will likely have their function impeded by a membrane that is too rigid. So whether we're talking about omega-3 in the context of mortality or in the context of brain function, omega-3 is awesome & extremely important. Let's now turn to the original thrust of this article, however, and dive into a comparison between fish oil and krill oil. These are the two most common sources, with the latter of which being a bit more expensive but arguably a superior option. Now, I know what you're thinking: there is no way omega-3 can do all of that stuff, I must be trying to sell you on some kinda snake oil! I hope so. I hope so, my friend. And that is because I'm a fan of irony: Snake oil, real snake oil at least, has actually been found to be a fat that is rich in omega-3 fatty acids. In fact, Chinese snake oil has been found to have even more of the anti-inflammatory goodness known as eicosapentaenoic acid than fish oil: on average snake oil is about 20% EPA, which is about 2% more than fish oil at 18%. [2] Krill Oil's Differentiating Characteristics There are a few key characteristics or facts that differentiate krill oil from fish oil in a way that  might influence the way you supplement. Krill oil has a higher a bioavailability due to most of its EPA and DHA fatty acids being attached to phospholipids, unlike the omega-3 fatty acids in fish oil which are either found in a triglyceride or ethyl ester form. One of the phospholipids found in krill oil (and fish) has been found to be the almost exclusive source for DHA found in the brain in recent mouse, rat, and piglet studies. This phospholipid, known as phosphatidylcholine, is generally not found in molecularly distilled fish oil although it is produced in the body. Krill oil contains a special antioxidant called astaxanthin, which is a carotenoid that fish oil does not contain. Molecular Distillation As A Point of Distinction It's important to understand that fish oil is usually modified by the process of molecular distillation, which allows EPA and DHA to be concentrated and removes contaminants like mercury. Krill oil is able to circumvent this processing altogether largely due to its lack of contamination characteristic of its position, which sits lower in the food chain. The omega-3 fatty acids EPA and DHA in fish are mostly in triglyceride form, meaning three fatty acids are bound to a glycerol backbone. Once fish oil is distilled it is no longer the same substance. After distillation the EPA and DHA is converted from triglyceride form into ethyl ester form by removing the glycerol backbone and replacing it with an ethanol backbone. At this stage it can be converted back into a triglyceride form by a process called re-esterification, which adds the glycerol backbone back onto EPA & DHA. [3] This secondary process of converting EPA and DHA back into triglyceride form is unique to higher-end brands of fish oil (like nordic naturals) and is done to deliberately increase the bioavailability of EPA and DHA fatty acids. Unfortunately, many of the fish oil supplements on the market are left in ethyl ester form after molecular distillation and the bioavailability of EPA and DHA in ethyl ester form is much lower than triglyceride form. [4] Krill oil contains EPA and DHA that are mostly present in phospholipids, including: phosphatidylcholine phosphatidylserine phosphatidylethanolamine A phospholipid is composed of a fat-soluble diacylglyceride and a water soluble phosphate group attached to an organic molecule (choline, serine, or ethanolamine in the previous examples). What's important to know about the phospholipids in krill oil is that they are far more bioavailable than fish oil's triglyceride or estyl ether forms. Phosphatidylcholine, in particular, is very important, but I'll elaborate more on that in a moment. Bioavailability of Krill Oil vs. Fish Oil There are two keys areas where omega-3 fatty acids can encounter problems, which affect its bioavailability and use by your tissues. First is absorption in the small intestine after ingestion. Second, is actual transport inside different tissues (such as the brain, heart, and liver) after intestinal absorption. First let's cover the differences in intestinal absorption of phospholipids (mostly found in krill oil), triglycerides (mostly found in fish oil, if industrially re-esterified), and ethyl esters (mostly found in fish oil, if it wasn't re-esterified). In order to be absorbed by the small intestine, the EPA and DHA from fish oil present in triglyceride or ethyl ester form must be broken down by pancreatic lipases (enzymes that break down triglycerides) into free omega-3 fatty acids (meaning they are cleaved from their backbone). The EPA and DHA in phospholipids from krill oil are also broken down into free omega-3 fatty acids in small intestine by a different class of enzymes called phospholipases (enzymes that break down phospholipids) but here is the important point: they do not necessarily have to be broken down because they can also form micelles which can be absorbed in their intact form. Ethyl esters are poor substrates for pancreatic lipases which means the EPA and DHA in ethyl ester form are not absorbed as well as in triglyceride form (since the ethyl esters are less able to complete the conversion into free fatty acids). While the EPA and DHA in triglycerides are more bioavailable than ethyl esters, they are not more bioavailable than phospholipids. There are two reasons for this: EPA and DHA in triglycerides can be broken down by gastric lipases in the stomach, which means some of the omega-3 fatty acids in fish oil are lost in the stomach and never make it to the small intestine for absorption into the bloodstream. Unfortunately, the most bioavailable component of fish oil (triglyceride form) is the form that is most susceptible to this, whereas the phospholipids (ie. phosphatidylcholine) found in krill oil are generally not broken down in the stomach. [3] Krill oil's phospholipids do not necessarily have to be broken down into free fatty acids by phospholipases in the small intestine since they can also be absorbed in their intact form by chylomicrons, which are the lipoproteins responsible for transporting omega-3 in the bloodstream. [5] Even though ethyl ester is the least bioavailable form, one trick that can help improve even its bioavailability is to eat it with an accompanying high fat meal (in other words, a meal rich in triglycerides). [6] How Much More Bioavailable Is Krill? About 40%. There is evidence demonstrating that omega-3 fatty acids are more bioavailable in krill oil.  When identical doses of EPA and DHA were given in either phospholipid form, triglyceride form, or ethyl ester form (molecularly distilled) to humans, EPA and DHA concentrations in plasma cholesterol were shown to be highest when in phospholipid form followed by triglyceride form and, lastly, ethyl ester form. [7]  In line with this, another study in which humans that were given krill oil containing 62.8% of the total amount of omega-3 fatty acids in fish oil, increased their plasma EPA and DHA levels to the same level as those in the fish oil group despite the fact that it was a smaller dose (by 37.2%). [8] Because the EPA and DHA concentrations in plasma cholesterol are indicative of the amount actually being absorbed in the small intestine and into the bloodstream, this suggests that EPA and DHA in phospholipid form is more bioavailable than triglyceride and ethyl ester is the least bioavailable. DHA from Krill Oil More Readily Transported to Brain Cells The concentration of EPA and DHA in plasma cholesterol is not necessarily indicative of the amount of these omega-3 fatty acid concentrations inside different cell types. So let's take a closer look at the mechanisms of transport inside different tissues starting with my favorite, the brain.      DHA is the most abundant fatty acid found in the brain, making up 10 to 20% of the brain's total lipid composition, which is 60% by dry weight. [9] Despite the fact that DHA is abundant in the brain, the mechanisms of how DHA crosses the blood-brain barrier have remained unclear for some time, up until recently. As it turns out, something called DHA-lyso-phosphatidylcholine is far more preferred by the brain compared to DHA in its free fatty acid form, which is what we have left over after triglyceride or ethyl ester DHA has been broken down by lipases. [10,11] But what is DHA-lyso-phosphatidylcholine? DHA-lyso-phosphatidylcholine is a byproduct of DHA in phosphatidylcholine after it is cleaved (by phospholipases) either in the small intestine or in the bloodstream. Since DHA in phosphatidylcholine is primarily found in krill oil and not fish oil, this means that krill oil is a great source for DHA-lyso-phosphatidylcholine while fish oil is not. [11] It seems as though DHA-lyso-phosphatidylcholine may be really important. In fact, studies have shown that DHA-lyso-phosphatidylcholine accumulates by 10-fold higher amounts in the brain than DHA in free fatty acid form. [10] This isn't a phenomenon specific to just rats, either. Another study demonstrated something very similar in piglets as well:  DHA is taken up into developing brains of piglets in phosphatidylcholine far more effectively than DHA in triglyceride form. [12] A Transporter Specialized for DHA-lysophosphatidylcholine So what is the mechanism? Why does the brain prefer DHA-lysophosphatidylcholine over DHA in free fatty acid form? A nature paper published in May 2014 found a specialized DHA transporter (called Mfsd2a) that transports DHA-lysophosphatidylcholine across the blood-brain barrier. They showed that mice engineered to lack this transporter had 60% less DHA in their brain compared to normal mice! [13]  Getting rid of this transporter ONLY affected DHA levels in the brain and not other tissues, such as the heart or liver... which, instead, has been shown to mostly accumulate DHA in its non-esterified form. [10] The one exception is red blood cells, which actually also prefers DHA-lysophosphatidylcholine which makes sense because DHA concentrations in red blood cells tightly correlate to actual DHA levels found in the brain. [14]  This last point actually makes a great argument for using red blood cell omega-3 content as an index for omega-3 sufficiency instead of the more common plasma cholesterol tests, but as of yet this type of test is not widely available on the market. Krill Oil Has Its Own Antioxidant: Astaxanthin One other unique aspect of krill oil is that, unlike fish oil, krill oil contains astaxanthin. That isn't to say that fish don't contain astaxanthin, common fish that eat zooplankton, such as salmon, do as well. However, insofar as we're talking about omega-3 supplements: astaxanthin is a carotenoid that is unique to krill oil and is not present in fish oil. Astaxanthin is produced primarily by phytoplankton, which biosynthesize the precursors lycopene and beta-carotene; zooplankton graze on phytoplankton and convert some of the beta-carotene to astaxanthin. Fish (such as salmon) and crustaceans (such as krill) eat the zooplankton and this is their source of astaxanthin. [15] Carotenoids, such as astaxanthin, are antioxidants that uniquely sequester a type of oxidation originating from singlet oxygen (which is produced from UV radiation) and they are also strong antioxidants against peroxyl radicals. [16] Singlet oxygen and peroxy radicals are very reactive and can damage lipid membranes, DNA, and proteins in your cells. All of these are fundamental biological causes of aging. (Note: for more information on this please see my video entitled, "Do Antioxidants Cause Cancer?"). Something cool about astaxanthin in particular is that it is one of the carotenoids that is easily absorbed into the human bloodstream. Astaxanthin has an amphipathic structure (both water soluble and lipid soluble properties), which allows it to accumulate in cell membranes. This a is a good thing, because DHA, which is very prone to oxidative damage, also accumulates in cell membranes where it is needed to play a critical role for the cell in membrane fluidity. Many antioxidants, such as glutathione, are produced and used inside the soluble portion of the cell but are not present in cell membranes. For this reason, getting a little astaxanthin with your omega-3 fatty acids may be a great way to uniquely protect that DHA as well as other polyunsaturated fats in the cell membrane from oxidation since it is localized to the same membrane region of the cell as DHA. Astaxanthin may also have other benefits on its own. For example, astaxanthin supplementation all by itself has been shown in humans to improve immune function while decreasing an important marker of inflammation known as C-Reactive Protein. [17] Astaxanthin also reduced DNA damage, hyperlipidemia, and oxidative stress by suppressing lipid peroxidation and increased HDL. [17-20] Oxidative stress, DNA damage, and inflammation are all important initiators of cancer, which I talked about in length in my video "Do Antioxidants Cause Cancer?" Astaxanthin as a supplement has also been shown to increase HDL-cholesterol and decrease triglycerides (suggesting it plays an important role in cardiovascular health), reduce the oxidation of cell membranes which has been known to play a role in skin aging, and been shown to actually improve crow's feet, elasticity, and transepidermal water loss. [21] In conclusion, astaxanthin supplementation may be beneficial for fighting against many degenerative diseases of aging, such as cancer, cardiovascular disease, stroke, diabetes, and neurodegenerative diseases. Summary Krill oil "beats" fish oil from many different perspectives: the EPA and DHA are more bioavailable as a consequence of phospholipids. One of the most compelling reasons krill oil is superior to fish oil is due to the fact that krill oil is a source of DHA-lysophosphatidylcholine, the preferred form of DHA in the brain. Additionally, krill oil comes with the added bonus of astaxanthin, which may also play a special role in the fight against aging that other antioxidants don't. One last novel feature that is specific to krill oil and not fish oil is that it is also a great source of other phospholipids such as phosphatidylserine, phosphatidylethanolamine which are abundant in mitochondrial membranes and neuronal cell membranes. In fact, the levels of these phospholipids in mitochondrial membranes and neuronal membranes decrease with age and this has been linked to neurodegenerative diseases such as Alzheimer's and Parkinson's Disease. How much do I take? The next question many of you might ask is how much to take. I personally take a lot of omega-3: in the past I've adjusted my fish oil dose to correspond to about 2 grams of EPA and 1 gram of DHA per day based on studies I'd read that seemed to suggest this might be a good therapeutic dose. What the ideal amount to supplement with krill oil is: I have no idea. This open for debate and something I'm not sure about. As of right now I tend to take some of both. I'm hoping that with the new discovery of this brain-specific transporter, clinical trials will use krill oil when trying to understand the effects of DHA supplementation on the brain. If I figure anymore out, I'll let you guys know. Until next time! Thanks for reading. We're a razor's edge from our second milestone! We're now at ~55% of the $4,500/mo milestone! Consider making a small, even infinitesimal Patreon pledge to support FoundMyFitness articles and videos. You can pledge as little as $0.25 per month... but if you do decide to pledge a little more to help us reach our milestones, we'll throw in a few Patreon members-only perks like:  Early content access The opportunity to influence what topics get picked next Access to Google Hangouts (limited slots) Click here to learn more about our milestones and how-to pledge! References 1. Danaei G, Ding EL, Mozaffarian D, Taylor B, Rehm J, Murray CJ, Ezzati M: The preventable causes of death in the United States: comparative risk assessment of dietary, lifestyle, and metabolic risk factors. PLoS Med 2009, 6:e1000058. 2. Graber C: Snake Oil Salesmen Were on to Something. Edited by. Scientific American: Scientific American; 2007. 3. Dyerberg J, Madsen P, Moller JM, Aardestrup I, Schmidt EB: Bioavailability of marine n-3 fatty acid formulations. Prostaglandins Leukot Essent Fatty Acids 2010, 83:137-141. 4. Neubronner J, Schuchardt JP, Kressel G, Merkel M, von Schacky C, Hahn A: Enhanced increase of omega-3 index in response to long-term n-3 fatty acid supplementation from triacylglycerides versus ethyl esters. Eur J Clin Nutr 2011, 65:247-254. 5. Cohn JS, Kamili A, Wat E, Chung RW, Tandy S: Dietary phospholipids and intestinal cholesterol absorption. Nutrients 2010, 2:116-127. 6. Lawson LD, Hughes BG: Human absorption of fish oil fatty acids as triacylglycerols, free acids, or ethyl esters. Biochem Biophys Res Commun 1988, 152:328-335. 7. Schuchardt JP, Schneider I, Meyer H, Neubronner J, von Schacky C, Hahn A: Incorporation of EPA and DHA into plasma phospholipids in response to different omega-3 fatty acid formulations--a comparative bioavailability study of fish oil vs. krill oil. Lipids Health Dis 2011, 10:145. 8. Ulven SM, Kirkhus B, Lamglait A, Basu S, Elind E, Haider T, Berge K, Vik H, Pedersen JI: Metabolic effects of krill oil are essentially similar to those of fish oil but at lower dose of EPA and DHA, in healthy volunteers. Lipids 2011, 46:37-46. 9. Yehuda S, Rabinovitz S, Mostofsky DI: Essential fatty acids are mediators of brain biochemistry and cognitive functions. J Neurosci Res 1999, 56:565-570. 10. Thies F, Pillon C, Moliere P, Lagarde M, Lecerf J: Preferential incorporation of sn-2 lysoPC DHA over unesterified DHA in the young rat brain. Am J Physiol 1994, 267:R1273-1279. 11. Croset M, Brossard N, Polette A, Lagarde M: Characterization of plasma unsaturated lysophosphatidylcholines in human and rat. Biochem J 2000, 345 Pt 1:61-67. 12. Liu L, Bartke N, Van Daele H, Lawrence P, Qin X, Park HG, Kothapalli K, Windust A, Bindels J, Wang Z, et al.: Higher efficacy of dietary DHA provided as a phospholipid than as a triglyceride for brain DHA accretion in neonatal piglets. J Lipid Res 2014, 55:531-539. 13. Nguyen LN, Ma D, Shui G, Wong P, Cazenave-Gassiot A, Zhang X, Wenk MR, Goh EL, Silver DL: Mfsd2a is a transporter for the essential omega-3 fatty acid docosahexaenoic acid. Nature 2014, 509:503-506. 14. Kuratko CN, Salem N, Jr.: Biomarkers of DHA status. Prostaglandins Leukot Essent Fatty Acids 2009, 81:111-118. 15. Andersson M, Van Nieuwerburgh, L., Snoeijs, P.: Pigment transfer from phytoplankton to zooplankton with emphasis on astaxanthin production in the Baltic Sea food web. Inter-Research Marine Biology Progress Series 2003:213-224 16. Naguib YM: Antioxidant activities of astaxanthin and related carotenoids. J Agric Food Chem 2000, 48:1150-1154. 17. Park JS, Chyun JH, Kim YK, Line LL, Chew BP: Astaxanthin decreased oxidative stress and inflammation and enhanced immune response in humans. Nutr Metab (Lond) 2010, 7:18. 18. Riccioni G, D'Orazio N, Franceschelli S, Speranza L: Marine carotenoids and cardiovascular risk markers. Mar Drugs 2011, 9:1166-1175. 19. Choi HD, Kim JH, Chang MJ, Kyu-Youn Y, Shin WG: Effects of astaxanthin on oxidative stress in overweight and obese adults. Phytother Res 2011, 25:1813-1818. 20. Yoshida H, Yanai H, Ito K, Tomono Y, Koikeda T, Tsukahara H, Tada N: Administration of natural astaxanthin increases serum HDL-cholesterol and adiponectin in subjects with mild hyperlipidemia. Atherosclerosis 2010, 209:520-523. 21. Tominaga K, Hongo N, Karato M, Yamashita E: Cosmetic benefits of astaxanthin on humans subjects. Acta Biochim Pol 2012, 59:43-47. About Dr. Patrick: Dr. Patrick has a Ph.D. in Biomedical Science and has done extensive research on aging, cancer, and nutrition. She is an expert on nutrition and metabolism and currently conducts clinical trials examining the positive effects of vitamin and mineral supplementation on metabolism, inflammation, and aging.

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