Monthly Archives: March 2016

Resistant Starch: Super Food

Resistant Starch – Secret Super Food?

Reference:  AJCN, 2005, AJCN 2005, International Jr Obesity

Have you heard of resistant starch? It’s been making the rounds and has even sparked some books. In its simplest explanation, it’s starch that isn’t easily digested. There are actually four different categories that have been sorted out so far. 1) starches attached to the indigestible cell wall of beans, seeds and some grains. 2) Starch in plantains, potatoes and bananas that is indigestible prior to heating and cooking because of its high content of amylose. Heating it makes it bio-available. 3) Retrograded starch. This type becomes resistant on cooling after cooking. This can be found in potatoes, some beans and grains. 4) The fourth type is industrially made by modifying corn starch.

It’s what resistant starch (RS) does in the body that makes it interesting. Starch is essentially long chains of glucose. Glucose is a molecular ring of 6 atoms which has six binding sites for attachment. When glucose molecules are attached to each other at the #1 and the #4 sites, they line up like beads and make a very tight package that is not easily digestible. This is called amyloseand is about 20% of many starches. This is the resistant stuff. 80% of starch has glucose branches every 20-30 molecules making a very branched chain, and enzymes can get in those branches and break them apart. This is called amylopectin, is very digestible and releases sugar into the blood vary rapidly. This is the stuff that makes potatoes, bananas and rice quite high in digestible starch.

Now, resistant starch turns out to do interesting things in your gut. It encourages the growth of different bacteria. Those bacteria produce n-butyrate, the main food of colonic cells. . In fact, they are the main source of n-butyrate. Did you get that? The right bacteria in your gut make the food that your colonic cells depend on. Your colonic cells aren’t fed by the nutrients in your blood as much as by energy from n-butyrate. Totally counterintuitive!

But that isn’t the half of it. Resistant starch improves insulin sensitivity. That is opposite to what you would expect. How does that work? It’s too complicated to dissect here but leave it to say, those short chain fatty acids also get into your blood, and participate in a whole cascade of effects, most importantly being more insulin sensitivity. Lower levels of insulin basically make it easier for fat cells to open up and share their calories. When that happens, you aren’t as hungry because you get calories from your fat. That’s called weight loss. Did you get that? Weight loss! RS increases magnesium absorption. Many folks report better mood and better sleep. Hmmm. Imagine that. The hypothesis is your gut makes serotonin, and when your gut is well fed, that makes you feel better.

Are there bad effects of RS? Well, yes. Some folks complain of bloating and gas. Some say they gain weight. That makes sense too when you consider that RS is only part of potatoes and bananas. When you eat the whole potato, you also get 80% amylopectin, the easily digested sugar.

WWW. What will work for me. I’m totally fascinated with the concept that our intestinal bacteria feed our colon, and they get their food from RS. I know we can measure butyrate on stool tests, and just about everyone is low. I want to watch this story and figure out how to get some into my diet without gaining weight or increasing my bad blood lipids. I’m not out eating more potatoes quite yet, but I did try a cold one yesterday.

Pop Quiz

1. Resistant starch is basically chains of glucose that we don’t have enzymes to digest, but our colon’s bacteria do. T or F

That’s it in a nutshell.

1. There are beneficial bacteria in your colon that digest RS and make it into gas that feeds your colon cells. T or F

Oops, you missed the point. False. Those bacteria make butyrate, a short chain fatty acid, that feeds your colon. It’s not a gas. But, some folks do feel gassy when they start eating RS.

1. A clear benefit of RS is that your insulin sensitivity goes up, which means your insulin levels go down, which is good. T or G

True. Fascinating. Not intuitively obvious.

1. Better sleep and calmer mood may be a side effect of RS. T and F

Yup. Might be worth a try if you want to buy the pure stuff and add that as a supplement to your diet.

1. Resistant starch has been well studied and fully characterized. T or F

Not at all. This story is just starting. There is no obvious money in it because it’s already out there. If it were a pill that could be patented, you would see it on the evening news and being sold for big bucks. As it is, its benefit is still being studied and no one hears much about it.

Lead’s Effect May Last LIFETIMES (plural)

Lead’s Effect May Last Lifetimes

Published:  March 21, 2016

Reference: Science News 2016, Translational Psychiatry

The recent controversy about lead in Flint, Michigan has raised the topic of lead poisoning again. Lead removal from America has been one of the public health victories of the last century.   We have gotten it out of our lead pipes, our house paint, our gasoline. It was only 1996 that lead was finally banned from gasoline. But did you know that it persists still in chocolate? In Nigeria, gasoline still has lead in it, and chocolate from Nigeria has up to 460 times the lead in it compared to the cocoa bean. Hence, eating many chocolate products gives children more lead than California says is safe.

Now, we are beginning to understand just how lead does its dirty work. It’s half life in blood is only about 30 days, but in your bone and teeth, where most goes, it hangs around for 25 years. Guilarte, in a study published last year in Translational Psychiatry, showed that baby rats fed tiny amounts of lead lost critical neurons in their brains that are essential for attention and memory, and gained dopamine receptors, in a pattern that fits with schizophrenia. They hypothesize that lead does its damage by replacing zinc. Zinc’s role in the cell is to help switch-proteins fold properly to turn on and turn off DNA.   Lead replaces zinc but doesn’t let the switches happen. Jacqueline Ordemann of Bates College proposed in the Journal Metallomics this year, that lead affects the switches in our brains that affect our sensitivity to schizophrenia, Alzheimer’s and Parkinsons, three brain diseases that have increased dramatically in the last century. Another author, Ruden, published a report in Scientific Reports in January this year showing that lead affects methyl groups on DNA in an atypical fashion. Methyl groups on DNA are how we turn off and on DNA replications. That is the means by which lead poisoning can be passed on to subsequent generations, through abnormal methylation of DNA, and subsequent altered copying of the DNA code.   Ruden compares our DNA to being the hardware of life, but methylation is the software that teaches the cell how to utilize the messages on the DNA. If lead messes that up, it is possible that the effect will last generations. To prove that, one would have to get a population exposed, and not exposed and follow it for generations. That is isn’t going to happen.

It is possible to pull lead out of the body, but not easily from the brain. Lead is not water soluble, so it gets soaked up into fat tissue. That’s what the brain is. And each cell in the brain is shrink wrapped with other cells, called glia, that make an added barrier to removing lead.   So little lead equalizes across that extra barrier that once lead is in you, it’s there to stay, at least in your brain. We may be able to remove it from your body fat, your bone marrow, or other body tissues, but your brain seems to be quite resistant.

Now that we understand some of the mechanisms of lead toxicity, it is incumbent on us to avoid the stuff rather than wait for more convincing research.

WWW.What will work for me? I’m helpless with chocolate. I love the stuff. Knowing what I know about lead, now, gives me resolve to avoid it until I see better evidence that the lead has been cleaned up.   Consumerlabs rates different chocolate sources for lead levels. I have chelated about 100 people in my practice for lead exposure and find that removing it improves thyroid function, white counts, concentration. And looking around my house, I found lead pellets for my air rifle, sitting on a shelf. I haven’t used them for years, but there they were, sitting on my shelf.


Pop Quiz

  1. Lead is a normal micronutrient needed for human metabolism. T or F

False. Go back to square one and read the article. It’s a toxin, through and through.

  1. We have banned most sources of lead in America over a hundred years ago. T or F

False. We got it out of gasoline only as of 1996, and many houses still have an undercoat of lead paint and our nations’ water supply comes through many pipes with lead, even though lead pipes were banned years ago.

  1. Lead alters the DNA in our cells, making for abnormal interpretation of the message on the DNA. T or F


  1. Lead lingers a long time in bones and teeth. T or F

True. Maybe as long as 25 years, or longer in brains.

  1. Chocolate has lead in it. T or F

True. I weep, I mourn, I deny, but it’s true. I’ve heard rumor that Lindt chocolate doesn’t. Nigeria has leaded gasoline, and that may be the source.

Nothing is More Interesting than Rapamycin

Nothing is More Interesting than Rapamycin

Reference: AntiOxid and Redox Signal 2015, Chris Kresser Podcast, Nature

Published:  March 14, 2016

Rapamycin? Sounds like an antibiotic. It is! And it might be the most interesting antibiotic ever.   What makes it interesting is that it impacts the mTOR pathway, which is the most primitive pathway of metabolism of all, applying to virtually every living creature. (mTOR means “mechanistic target of rapamycin”)   Rapamycin is the only known chemical that modulates aging in all four model species: yeast, worm, flies and mammals.

Rapamycin is so named because it was found on the island Rapa Nui, which is what natives call Easter Island. The strain of Stretomyces (a fungus) in which it was found was unique to Easter Island. A research group from McGill University went there looking for new strains of fungus from which to extract antibiotics.   Suren Sehgal was the researcher working for Ayerst Labs who isolated it and found it to be an amazing cure for athlete’s foot. But Ayerst Lab went belly up so Sehgal saved the rapamycin and hid it in his freezer until Wyeth Labs bought out the rights of the company.

But it was not until the early 90s that a PhD student named David Sabitini doing research on stroke reperfusion used rapamycin as a control drug. He refused to do the easy study that his supervisor wanted him to work on, and instead went off on a tangent. Sabitini wanted to figure out just how rapamycin worked, and ended up discovering the mTOR protein complex.   MTOR turns out to be a master regulator of protein translation, cell growth, and proliferation.   And for a whole host of reasons, these actions end up being smack dab in the middle of understanding how cancer gets out of sync, and how aging wears us down.

So, just how does rapamycin work?   How does mTOR work? Rapamycin works by flipping a switch in cells that sense nutrients in the environment. The cells think they are starving. Crisis! Hunker down and go into slow mode. Sabatini also found RAPTOR, (rapamycin associated protein) that regulates cell size in response to the level of environmental food supply. And then there is GβL that regulates how Raptor and mTOR interact. There is mTORC1 and mTORC2 which are in different tissues in different concentrations, but all on the same theme.   We now have a chemical that induces resistance to aging through the same pathway as calorie restriction. Calorie restriction only works well if started at birth. Rapamycin adds its benefit when ever it’s started.

Just what could Rapamycin do for us? Right now, we aren’t really sure except that it is an amazing research tool that is helping unpack the complexities of human biology. In mice we know that intermittent dosing of rapamycin prolongs life substantially, mimicking calorie restriction. We do know that nutrient manipulation in cancer is incredibly powerful, and this approach may lead us to a path that confirms exactly how that works.

WWW. What will work for me? The clear message is that calorie restriction slows down aging. We know that autophagy (cleaning out old, used up cells) is enhanced by calorie restriction, and it’s effect is accelerated by rapamycin. That is something everyone should be interested in because lousy autophagy is central to Alzheimer’s. And green tea (EGCG) inhibits mTOR. That’s part of its effect on cancer. So, I’m paying attention to mTOR. I’ve almost switched all my tea to green. Thought you should too. Eventually, we may all be taking it as our morning mTOR stimulation.


Pop Quiz

  1. Rapamycin was named after a fungus found on Easter Island? T or F

That’s it, Rapa Nui

  1. Rapamycin is a powerful anti-fungal antibiotic that appears to block your body’s sensor of calories? T or F                                                                                                                                 Perfect.
  1. MTOR is the protein complex that inhibits rapamycin. T or F

False. mTor is one of several proteins that rapamycin inhibits. That’s vice versa.

  1. Rapamycin induces longer life in every model of animal it’s been studied, from yeast to mammals. T or F


  1. Calorie restriction can prolong life? T or F

True, but probably more effectively starting earlier than later.

  1. Rapamycin may have beneficial effects on aging, cancer, Alzheimer’s, diabetes? T or F


Senescent Cells and Living Longer

To Live Long, Senescent Cells Gotta Go

Reference: Nature Feb 2016,

Your cells in your body are constantly dividing, up to a limit. Once they reach that limit, they stop. They are now “senescent”.   They have gotten old. Instead of doing their job, they are in the way and stop performing. Worse, they pump out all sorts of inflammatory compounds.   And that plays a role in your aging.   Hayflick described this limit some 40 years ago and it has been challenged, but continues to make sense as we come to understand how we age.

As those cells get “senescent”, they build up a protein, p16, that tells them to commit Hari-Kari, or apoptosis.   P16 has been most studied in cancers where it appears to limit the ability of the cancer to multiply.   Turning it off is useful. Turning it off slows down aging. Which means getting rid of those cells might slow aging.

This is a useful line of attack for cancer, where cells don’t know to age and live way too long. And it is a useful concept to attack when we consider human aging.

Here is what this paper shows.   The researchers, Jan van Deursen, of the Mayo Clinic, and her team, added a snip of DNA to mice to manufacture a suicide protein when p16 shows up.   When p16 gets made, so does the suicide protein. But the protein only works when it has another chemical cofactor that is not naturally present in mice.   Then they waited until the mice were 60 years old in human terms; one year old in mice terms.   At that point they started injecting the partner chemical every 3 days.   That would make senescent cells that had started manufacturing p16 turn on the suicide gene. That would make the senescent cells die and be gotten rid of.   No inflammation, no damage to surrounding tissue.   The mice lived about 25% longer than the normal mice.   In human terms, that would be adding 20 years of life to your life span.

This sounds like a major leap forward in the anti-aging realm. But there is a very long way to go.   This is just showing us that we have a mechanism that can be manipulated in mammals to prolong life.   There are many barriers.   Inserting a gene into your DNA isn’t so easily done, quite yet. The technology is galloping ahead though, so it may not be long.

And, there are other problems. Senescent cells are required for wound healing.  They make PDGF-AA, which is a wound healing accelerant.   You can’t just turn off one function of cells. Somehow, in the mystery of how we all fit together, we have found useful features in senescent cells. That may explain why they have been allowed to hang around. The benefit is that you fix a cut, or a wound. The downside is you die, just a bit later.   Well, then, if you need surgery or get a wound, stop injecting the partner chemical and presto, you go back to healing again.

Is this ready for prime time? Humans? Not by a long shot. But at the speed at which medical research is racing ahead, it sure makes for interesting reading.

But remember, you can already add 14 years to your life with a very simple strategy. The Harvard Professional Men’s study showed that getting your BMI to 25, exercising every day, not smoking, eating more vegetables and less sugar and flour and red meat, and a glass of wine a day and you add 14 years to your live. Start with that. By the time you’ve used that up, p16 and friends might be ready.

WWW. What will work for me.   I’m curious. I want to understand this stuff. I think my life time may see this advance.   But if I’m hanging around much longer than I want, hmmm.   I want control of when I exit too.


Pop Quiz

  1. Mice can live 25% longer if they can be programmed to clear out their senescent cells.   T or F

That’s it in a nutshell.

  1. Senescent cells spew out inflammation, damaging tissue around them. T or F

Again, right on

  1. You need senescent cells to help wound healing. T or F

That’s their benefit.

  1. This technology might be ready for humans in a year or two. T or F

Whew, not likely. But this line of research may provide a path forward. We need more discoveries added on first.

  1. Time to buy your long term care policy quick? T or F

Whoa Nellie. Not so fast. We have dozens of ethical and cellular engineering issues to work out before we get there.