Women’s Health, Inflamaging and Belly Fat

Tasneem Bhatia, MD spoke (MP3) at the American Academy for Anti-Aging Medicine World Congress in December.  Her presentation offered a busy clinician's insights into managing many women's complaints, offering real solutions that are based on treating the underlying causes rather than just the symptoms.

  • The gut microbiome absolutely impacts women's hormones!
  • They want Hormones… Before we have a conversation about Hormone Replacement, "What's happening in your gut?"  They get this shocked look on their face, like this is not why I visited your office  7:41
  • …In the last couple of years, there's been this surge of young women (in their 20's and early 30's) coming in …
  • Recipe for Disruption of the GUT at 32:00
  • Protocol for Leaky Gut at 35:00
  • Belly Fat / inflammation: "80% food and gut, and 20% exercise"

I judge that this talk is a good sign that some MDs are becoming aware of the Gut/Health relationship and are asking some of the right questions. 

Impressions from “Health and Fitness Expo”

I spent yesterday afternoon at the Total Health and Fitness Expo in Sacramento.
 

The Good:

  • Lots of people care about their health and are doing what they think best to help/support/improve it
  • Lots of people working to support others in getting and staying healthy
  • Many people are willing to put a lot of effort into getting fit

The Questionable:

  • Many people throwing weights and/or their bodies around in ways likely to produce injury
  • Many people advocating eating six carbohydrate-laden meals per day to "keep up one's energy"
  • Someone connected with the American Diabetes Association promoting "Healthy Eating for Diabetics" that recommended eating majority of calories from carbohydrates
  • A "Pilates and Yoga" studio promoting classes with names like "Bikini Butt".  Their display featured a giant kettlebell which I thought must weigh at least 70 pounds but turned out to be hollow, weighing perhaps just 20 pounds.

 

Get Young Club pre-launch

Welcome!

I’m excited to have begun inviting interested (and interesting) selected people to join this exclusive club where we can share the benefits of the exciting, emerging technology of Age Reversal!

A new and improved version of this website is currently being built to better serve our mission.

At the same time, we have a the  Get Young Club – FaceBook group for those of you who like Facebook.  For those of you who prefer to avoid Facebook (and keep your privacy), we’re building this site to support that… It will soon be members-only.

As our stem cells age, how much DNA damage accompanies Telomere Shortening?

I question enough of Dr. Park's assertions in his recent post that I'm quoting it below and adding my comments in blue italics:

Dr. Ed Park wrote: "Every New Year’s Guide to aging

Out with the old year and the old ideas and in with the new. I would like to offer my understanding of why we get old and sick and tell you what the future holds for defeating these scourges


bad-photocopy-template-05-o

1) You started with only one ‘perfect’ copy of DNA in your chromosomes when you were a single cell fertilized egg. Since then, each copy has made successive generations progressively worse

dna_damage_never_toleratedThe telomeres do shorten, and this could easily be a clock that signals/directs Programmed Aging, but Dr. Mike Fossel  just wrote that DNA copying is robust: "Damage is never tolerated"

 


 

7292) There is no way to go back and look up the master copy and proofread and correct any newly minted cells to that standard of perfection. That said, custom stem cell differentiation will be available some day from your stored infant cord blood or adolescent ovarian/testicular biopsies.

When coupled with in situ senescent stem cell detection and destruction, we will have truly harnessed regenerative medicine.

But if the copies are in fact not damaged at the DNA level, but only "Epigentically aged" via signals driven by short telomeres, then lengthening the telomeres could reverse the damage.

 

 


 

5.2 Queenbee_RGB

3) We are eating off of ‘paper plates’ for most of our lives. In other words, the cells that make up most of our body and that we burn through rapidly are not the immortalized queen bee stem cells but rather throw-away drone bees and can only divide a finite number of times due to the Hayflick Limit

These queen bees are replenished by relatively younger ones frozen in cartilage known as mesenchymal stem stems. For more info read my book, Telomere Timebombs: Defusing the Terror of Aging


 

png4) Axiom #3 is a good thing because immortalized species with too many stem cells like trees, lobsters, and jellyfish grow really large

 

 

 

 

 


5) The more times stem cells copy themselves the greater the accumulation of little errors from transcription and the higher the likelihood of cataclysmic errors from end-to-end fusion and nondisjunction that result from the joining of ‘naked’ telomere ends that the DNA repair team can’t distinguish from a chromosome break. Again, this begs the question of whether there are in fact many transcription errors before telomere shortening leads to catacylsmic errors from end-to-end fusion and nondisjunction.  Where is the evidence for "many transcription errors" whlle telomere length is still sufficient?

3.2 TRAPEZE CHROMOSOMES_CMYK copy


6) You can’t be old when you’re young because you have too high a reserve of genetically intact replacement stem cells


7) You can’t easily look younger even with telomerase activators because your cells are made from master copy queen bees that are already genetically damaged and have epigenetic modifications that are also transmitted

Again, I accept the epigenetic modifications in the [aged] master copy queen bees, but where is the evidence for "already genetically damaged"?  Is Fossel wrong in his claim that DNA transcription / repair is extremely robust?


8) Cell replication, cell damage and destruction, and inflammation are not inherently bad if you maintain a huge reserve of high genetic integrity stem cells with long telomeres


9)  We actually depend upon cells both, stem and non-stem, to have intact self-annihilation from multiple mechanisms.  One of the primary ones is mediated by the “watchman of the genome”, P53, which triggers oxidative damage via poking holes in mitochondria. This hallmark of a an old an apoptotic cell is still mistaken for the cause, not result of aging

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10) Fixing damaged cells or tricking them to act younger is much less feasible and efficient than maintaining their genetic integrity by keeping the undamaged pool of stem cells healthier for longer via telomerase activity

Yes!  Prevention is better than cure.  But if we're dealing largely with Epigenetic changes, they are much easier to reverse than DNA damage. 

obos


 

So given these principles, the extreme health and longevity in the year 2116 will look like the following (may we all be around to benefit)…

1) banking cord blood for your newborn  Great option for those as yet unborn.

2) getting great sleep (the time when your cells heal and or replace themselves)  I can do that!

3) avoid excessive inflammation and cell destruction (smoking, drinking, excessive exercise) I can do that!

4) enhance telomerase activity with supplements, grateful abundant thinking, and humor. I can do that!

5) questioning anyone who tries to sell you a theory of aging that ignores replicative senescence, which is the only explanation that has natural models of premature aging, experimental evidence of age reversal, and thousands of articles linking disease of aging to shortened telomeres I can do that!

6) questioning anyone who asserts that DNA copying errors are as common as "noise accumulation" with an [analog] photocopying machine.


My gratitude to my friend Dr. Ed Park for stimulating me to write this response to his thoughtful post!

High Intensity Slow Training – aftermath

Post-workout portrait - I look tired and a bit dazed

I’m just back home after my 7th High Intensity Slow Training session.  Whew!

Even though my muscles were only under load for about eight minutes, I’m feeling drained, altered and a bit “wobbly” after my session tonight.  My friend Mark was encouraging me to really give it my all, and I feel like I did!

My goal was to give my body a stimulus to grow stronger, and I think I accomplished that!  Ugh!  Even sitting here at my desk feels like a lot of effort right now.  (Maybe the giant sausage and eggs breakfast 90 minutes before the workout contributed to this feeling I have?)

My numbers for weight and time have improved significantly but I feel like I may be plateaued somewhat with the one week rest interval and wonder if I should try increasing my rest interval to ten days or even two weeks – I want to give my body the time and rest it needs to make the adaptation!

The Obstacle

Pondering the Obstacle, I recall this quote from Michael Fossel:  (emphasis mine)

   "The assumption — shared by the public, scientists, and researchers — has been that aging is a simple, passive accumulation of damage for which there is no realistic intervention.  Aging can't be reversed and age-related diseases can't be cured.  Age-related diseases can only be endured or, at best, treated symptomatically or cosmetically.  You can't change your genes, nor can you avoid the passage of time.  We can cure or prevent many infectious diseases, but age-related diseases are everyone's fate.  Que sera, sera.

    With most pivotal advances in human history, the major obstacle has been the assumption that change was impossible. Such assumptions are always self-fulfilling. We only make progress when the thoughtless assumptions are shattered by thoughtful insight.  In this case, the insight is that aging and its diseases are the complex, dynamic result of gradual changes of gene expression, the effects of which are largely reversible, and that telomere elongation is an efficient point of intervention in aging and age-related diseases."

 Michael Fossel  Dr. Michael Fossel, The Telomerase Revolution: The Enzyme That Holds the Key to Human Aging…and Will Soon Lead to Longer, Healthier Lives, page 77

Born in 1950, Michael Fossel grew up New York, and lived in London, Palo Alto, San Francisco, Portland, and Denver. He graduated cum laude from Phillips Exeter Academy, received a joint BA (cum laude) and MA in psychology in four years from Wesleyan University in Connecticut, and, after completing a PhD in neurobiology at Stanford University in 1978, went on to finish his MD at Stanford Medical School in two and a half years. He was awarded a National Science Foundation Fellowship and taught at Stanford University, where he began studying aging, emphasizing premature aging syndromes. Dr. Fossel is a Clinical Professor of Medicine at Michigan State University.
He is a Fellow of the American College of Emergency Physicians, and a member of numerous scientific organizations including the American Association for the Advancement of Science, the American Aging Association (he was their executive director and serves on their board of directors), the American Gerontological Society, the American Society on Aging, and the American Geriatrics Society, among others.
He has lectured at the National Institute for Health, the Smithsonian Institute, and at universities and institutes internationally. He was founding editor of the Journal of Anti-Aging Medicine. His numerous articles on aging and ethics in the Journal of the American Medical Association, In Vivo, and other academic journals have sparked discussion and frequent calls for him to speak worldwide to both medical groups and the general public. He is frequently interviewed regarding aging by major media in the US and worldwide.
In 1996, Dr. Fossel published Reversing Human Aging, discussing the cellular causes of aging, how the process can be altered, and the social and financial implications of reversing human aging. The book was reviewed favorably in national full page newspaper articles and in Scientific American. It has now been published in six languages. He has appeared on Good Morning America, ABC 20/20, NBC Extra, Fox Network, CNN, the BBC, the Discovery Channel, and regularly on NPR.
His textbook, Cells, Aging, and Human Disease, was published in 2004 by Oxford University Press. An extensive look at the field, with well over four thousand up-to-date references, it reviews the entire fields of telomere biology and cell senescence as they apply to human clinical diseases and aging. It includes in depth discussions of Alzheimer's disease, the progerias, atherosclerosis, osteoporosis, immune senescence, skin aging, and cancer, as well as the potential for fundamentally new therapies for these diseases.

How Short Telomeres Cause Cancer

In the Dec 17 issue of Cell, researchers published results showing how short telomeres ("telomere crisis") can lead to cancer.  I judge that this helps confirm that my strategy of Telomerase Activation is helping prevent future cancers.  It also helps to confirm Dr. Ed Park's "Stem Cell Theory of Aging" and his "Telomere Timebomb theory of cancer".

Science News article (highlights mine):

Experiments explain the events behind molecular ‘bomb’ seen in cancer cells

Since scientists have begun sequencing the genome of cancer cells, they have noticed a curious pattern. In many different types of cancers, there are cells in which a part of a chromosome looks like it has been pulverized, then put back together incorrectly, leading to multiple mutations. For years, this phenomenon puzzled scientists. But new research from The Rockefeller University suggests an explanation for this strange molecular explosion that serves as a precursor to cancer.

“The ‘old’ idea in cancer is that it arose from a first bad mutation, and then a second mutation, and a third, and so on, until the cells divide uncontrollably, leading to cancer,” says Titia de Lange, Leon Hess Professor and head of the Laboratory of Cell Biology and Genetics, who led the study. “This is a whole new view of how cancer can arise—a bomb goes off in part of a chromosome, and you get multiple mutations at the same time. These latest findings reveal the molecular details behind that bomb.”

Tug of war: A chromatin bridge is formed as cells whose chromosomes are fused attempt to divide. The resulting daughter cells contain damaged DNA, which may serve as a precursor to cancer.

Tug of war: A chromatin bridge is formed as cells whose chromosomes are fused attempt to divide. The resulting daughter cells contain damaged DNA, which may serve as a precursor to cancer.

 

 

 

The study, published December 17 in Cell, describes the cellular events leading up to the phenomenon dubbed chromothripsis. However, these insights into the origins of chromothripsis came from an investigation into another molecular event that can lead to cancer, known as telomere crisis.

Telomere crisis results when the protective caps at the end of chromosomes, known as telomeres, become shortened as a result of cell divisions. With less DNA present in telomeres, it becomes harder to prevent separate chromosomes from attaching to each other. If those abnormal cells survive and continue to divide, they can give rise to cancer.

The researchers recreated telomere crisis in human cells by blocking the protein complex that prevents telomeres from fusing and disabling some of the molecular pathways that protect cells from turning cancerous. First author John Maciejowski, a postdoc in de Lange’s lab, filmed the events that followed.

For a long time, researchers believed that once two chromosomes fused together at their telomeres, they would eventually break apart during cell division. But the researchers found that’s not what happened at all. Instead, cells with fused chromosomes continue to divide with their chromosomes attached. Once division is complete and the new daughter cells try to move away from each other, the piece of chromosome they share becomes stretched, forming what’s known as a chromatin bridge. “I think of it as a balloon that’s been pinched in the middle, and the two outer circles are pulling away from each other,” says de Lange. “Or like a tug of war, and each cell represents the opposing team, and the rope gets stretched and stretched and stretched.” The chromatin bridge can reach 0.2 millimeters—an unheard of size at the cellular level.

Eventually, that bridge is broken down by one of the enzymes designed to target unfriendly DNA, such as that from viruses. And here, the researchers got a surprise—they discovered the enzyme that degrades the bridge DNA, TREX1, is normally present outside the nucleus that contains chromosomes. But as the two attached cells march away from each other, stretching the bridge DNA, that tension creates tiny tears in the membrane surrounding the nucleus, through which TREX1 enters and breaks down the chromatin bridge.

Once TREX1 causes the chromatin bridge to disintegrate, the two daughter cells spring away from each other. Each carries some of the bridge’s DNA fragments, which the cells then try to put back together. Some cells die from the trauma of this event, but others survive and divide, spreading the damaged DNA, which may contain shuffled portions, or have lost some of the genes that suppress cancer. In other words, this chain of events creates chromothripsis.

“The findings will hopefully help inform scientists’ understanding of the early molecular events that can lead to cancer, which may one day inform new methods to diagnose early stages of the disease,” says de Lange.

De Lange and Maciejowski collaborated on this project with Peter Campbell and Yilong Li from the Wellcome Trust Sanger Institute in Cambridge, UK, as well as Nazario Bosco at Rockefeller.

 

 

 

This confirms Dr. Ed Park's theory.  He writes:

http://www.rechargebiomedical.com/wp-content/uploads/telomeretbrock.jpg

His "Cancer Pyramid" illustration helps make it easy to understand:

http://www.rechargebiomedical.com/wp-content/uploads/6.3-cancer_pyramid_RGB1.jpg

These new results seem to show a way that failure of telomere protection "gets around" the p53 "Watchman of DNA" above.

Meanwhile, the result fits in with his most general and elegant "Stem Cell Theory of Aging":

There is only one disease with a thousand faces.

            -Dr. Ed Park (de facto, anonymously)

 

6.2-onedisease_RGB

Looks to me like Occam's razor might apply here!

– Jerome postie-media-6

Why I’m starting this blog

For weeks now, I've realized that I want a place to host the wonderful community that is forming around all the wonderful discoveries being made in the field of "Getting Younger".

Proposed Topics include:

  • Body

    • Telomere Lengthening
    • Telomerase Activation
    • Telomerase Gene Therapy
  • Metabolic Conditioning

    • Strength Training
  • Balance Training

    • Yoga
    • Pilates
  • Flexibility

    • Yoga
    • Pilates
  • Mind

    • Meditation
    • Positive Thinking
  • Spirit

    • Meditation
  • Science

    • Theories of Aging
    • Research Results
    • Telomere Theory of Aging
  • Community

    • Sharing ideas
    • Discussion
    • Mutual support
    • A "Hand up" culture

postie-media-6postie-media-7 

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