Category Archives: Anti-Aging Medicine

Question: You usually write about legal concerns, but I would like your opinion on a medical issue. I am getting older but still feel like I am in relatively good health. Every now and then when I see my doctor, I might ask about achy knees or tell him that I am more tired than usual. He usually responds by saying that it is to be expected as we age or, worse yet, he tries to give me a prescription! I know things are changing in the medical world and I wish my doctor would take a more proactive approach to keeping me healthy rather than writing me a prescription to treat aches or pain. Am I unrealistic to think that I can age better if I have access to the right medical advice?

Answer: As a senior advocate, I am open to addressing all types of senior concerns and healthy aging is at the top of my list of interests. Thank you for the question! You are right to be dissatisfied if your doctor responds that aches and fatigue should be expected as we age. There are literally daily advances being made in the anti-aging field and gaining access to the best and most researched wellness practices is essential for all of us if we want to stay healthy for as long as possible. I believe we can all agree that spending our last 10 or 20 years chronically ill before dying is an expensive nightmare we should all strive to avoid.

Over the past 25 years, leading scientists and clinicians have been researching and developing ways to personalize medicine based on a patients specific needs. Research shows the critical influence that diet, nutrition, lifestyle choices and environmental toxins have on the development of chronic diseases such as diabetes, heart disease, Alzheimers and cancer. Anti-aging or functional medicine doctors recognize the importance of establishing a patient-empowered health care system centered on prevention, early intervention of disease and optimal wellness throughout life rather than focusing on post-diagnosis, pharmaceutical-based care later in life when chronic illnesses may have already gained a foothold.

The Institute of Functional Medicine is a global organization seeking to advance Functional Medicine by partnering with academic medical centers, hospitals, universities, technology companies and our everyday doctors. You can find a list of functional practitioners at their website: IMF.org. David Sinclair, Ph.D., a professor of genetics at Harvard Medical School, has been researching aging for more than 20 years and recently released a book, Lifespan: Why We Age and Why We Dont Have To. Sinclair proposes that aging is a disease and, as such, is treatable and preventable. Also, self-proclaimed biohacker, Dave Asprey, recently released Superhuman: The Bulletproof Plan to Age Backward and Maybe Even Live Forever. Aspreys book is an easier read on the topic of anti-aging but, both books pave the way toward a new way to view aging.

We are right to question our doctors advice if we feel it is not addressing the problem and only treating symptoms. Our health is our greatest asset just ask anyone who is no longer healthy! Keep researching, reading, learning and be open to the possibility that through exercise, correct nutrition and personalized medicine it may be possible to stay healthy much longer.

Liza Horvath has over 30 years experience in the estate planning and trust fields and is a Licensed Professional Fiduciary. Liza currently serves as president of Monterey Trust Management. This is not intended to be legal or tax advice. If you have a question, call (831)646-5262 or email liza@montereytrust.com

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Liza Horvath, Senior Advocate: Age better with the right medical attention - Monterey Herald

LOS ANGELES, Dec. 11, 2019 (GLOBE NEWSWIRE) -- ChromaDex Corp. (NASDAQ:CDXC) today announced the launch of Tru Niagen Pro 500, the largest daily serving of its patented nicotinamide riboside (NR, or Niagen) ingredient in the world. The product will be available exclusively through licensed healthcare practitioners in the United States, launching this weekend at the American Academy for Anti-Aging Medicine (A4M) Annual Meeting in Las Vegas, NV.

This new product will allow practitioners to provide a unique product to their patients who want more energy and improved cellular health, says ChromaDex CEO Rob Fried.

ChromaDex maintains a growing network of healthcare practitioners who distribute Tru Niagen products to their patients and is also partnered with Natural Partners Fullscript for additional distribution.

We are pleased to launch this new product exclusively through the healthcare practitioner channel, says ChromaDex Chief Scientific Officer Dr. Matthew Roberts. This new product launch marks a major milestone in a year already characterized by several new significant scientific publications, human clinical data, and regulatory approvals around the world for ChromaDex.

Niagen is the only commercially available NR which has twice been successfully reviewed under U.S. Food & Drug Association's (FDA) new dietary ingredient (NDI) notification requirement and has also been successfully notified to the FDA as generally recognized as safe (GRAS). ChromaDex has also secured regulatory approvals on its patent-protected ingredient in Canada, the European Union, and Australia.

For additional information on the science supporting Tru Niagen, please visit http://www.truniagen.com.

About TRU NIAGEN:TRU NIAGEN is a branded dietary supplement brought to market by key nicotinamide riboside chloride innovator and patent holder, ChromaDex. NIAGEN nicotinamide riboside chloride (NR), also supplied by ChromaDex, is the sole active ingredient in TRU NIAGEN. Multiple clinical trials demonstrate NIAGEN is proven to boost NAD (nicotinamide adenine dinucleotide) levels, which decline with age. Only NIAGEN has twice been successfully reviewed under FDA's new dietary ingredient (NDI) notification program, and has also been successfully notified to the FDA as generally recognized as safe (GRAS).

About ChromaDex:ChromaDex Corp. is a science-based integrated nutraceutical company devoted to improving the way people age. ChromaDex scientists partner with leading universities and research institutions worldwide to uncover the full potential of NAD and identify and develop novel, science-based ingredients. Its flagship ingredient, NIAGEN nicotinamide riboside chloride, sold directly to consumers as TRU NIAGEN, is backed with clinical and scientific research, as well as extensive IP protection. TRU NIAGEN is helping the world AGE BETTER. ChromaDex maintains a website at http://www.chromadex.com to which ChromaDex regularly posts copies of its press releases as well as additional and financial information about the Company.

Forward-Looking Statements:This release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities and Exchange Act of 1934, as amended. Statements that are not a description of historical facts constitute forward-looking statements and may often, but not always, be identified by the use of such words as "expects", "anticipates", "intends", "estimates", "plans", "potential", "possible", "probable", "believes", "seeks", "may", "will", "should", "could" or the negative of such terms or other similar expressions. More detailed information about ChromaDex and the risk factors that may affect the realization of forward-looking statements is set forth in ChromaDex's Annual Report on Form 10-K for the fiscal year ended December 31, 2018, ChromaDex's Quarterly Reports on Form 10-Q and other filings submitted by ChromaDex to the SEC, copies of which may be obtained from the SEC's website at http://www.sec.gov. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof, and actual results may differ materially from those suggested by these forward-looking statements. All forward-looking statements are qualified in their entirety by this cautionary statement and ChromaDex undertakes no obligation to revise or update this release to reflect events or circumstances after the date hereof.

ChromaDex Media Contact:Alex Worsham, Senior Director of Global Corporate Communications310-388-6706 ext. 689alexw@chromadex.com

ChromaDex Investor Relations Contact:Brianna Gerber, Vice President of FP&A and Investor Relations949-419-0288 ext. 127briannag@chromadex.com

A photo accompanying this announcement is available at https://www.globenewswire.com/NewsRoom/AttachmentNg/f993967a-6441-4840-a4c7-c0f714c01374

Tru Niagen Pro 500

Largest daily serving of ChromaDex's patented NR Niagen

Link:

ChromaDex Launches Tru Niagen Pro 500, the Largest Serving of Patented Nicotinamide Riboside Available WorldwideTru Niagen Pro 500 to be distributed...

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Anti-Aging Medicine Market : Future Innovation Strategies, Growth & Profit Analysis, Forecast by 2018 - 2026 - The Market Expedition

For the first time, we are starting to see research that targets aging as a health condition in and of itself. Finding ways to regulate those "longevity gene" pathways referenced by Lipman above (specifically the mTOR, AMPK, and sirtuins) is central to scientists' work in identifying lifestyle habits, nutritional compounds, and future drugs that could slow and even treat (yes, treat) aging.*

As Sinclair views it, aging is most definitely a disease, and the FDA classifying it as such will help the field move forward even faster, allowing for more research and development of drugs to target processes thatlead to age-related disease. "The definition of a disease is that over time you lose function, you become decrepit, disabled, and eventually, if it's a bad disease, you die from it," says Sinclair. "That sounds a lot like aging, right? If you go to the medical dictionary, the only difference between aging and a disease is that a disease affects less than half the populationand that 50% cutoff is completely arbitrary."

How likely is that to happen? In 2018, the World Health Organization classified aging as a disease and added it to the International Classifications of Diseases system. And right now, scientists at the Albert Einstein College of Medicine are examining the anti-aging effects of metformin in the Targeting Aging With Metformin (TAME) study. If researchers can show significant benefits of metformin in delaying problems such as cancer, dementia, stroke, and heart attacks, the FDA may consider classifying aging as a treatable condition.

But why study metformin? This widely prescribed diabetes drug, derived from compounds in the French lilac plant, has been noted for its benefits beyond diabetesand Sinclair predicts it will be the first drug prescribed specifically to treat aging. Turns out, "metformin had a protective effect against cancer, heart disease, and frailty in patients taking the drug for long-term diabetes treatment," says Sinclair. "Which sounds a lot like a molecule that can slow aging." Animal studies have also confirmed that metformin can improve life span, and, more importantly, health span in mice. And, in a first-of-its-kind study in humans published in September 2019, researchers were actually able to take 2.5 years off participants' biological clock using a combination of metformin, dehydroepiandrosterone (DHEA), and growth hormone.

Experts believe metformin may activate similar pathways as caloric restriction to stimulate autophagyor cellular cleaning. This cellular upkeep is believed to be a key factor in extending health span. "It's a relatively safe AMPK pathway activator, and that's thought to mimic the effects of fasting and exercising," says Sinclair, who takes metformin daily as part of his healthy aging regimen.

Excerpt from:

Why We Aren't Anti-Aging, We Are Pro-Healthy Aging - mindbodygreen.com

Top Atlanta area plastic surgeon, Dr. Myla Bennett, is excited to offer CoolSculpting at her luxurious medical spa facility.

JOHNS CREEK, Ga., Dec. 11, 2019 /PRNewswire-PRWeb/ -- Dr. Myla Bennett is a highly-skilled plastic surgeon, skincare expert and founder of Ederra Bella Plastic Surgery and Medical Spa in Johns Creek, Georgia. In an effort to continue to provide advanced treatment options for patients, Ederra Bella is now offering the CoolSculpting procedure. It is the only FDA-cleared fat reduction technology to use controlled cooling to safely target fat cells in areas including the abdomen, thigh and flank areas. Once the targeted fat cells are eliminated from the body, they are gone for good. More than a million CoolSculpting procedures have been safely administered worldwide with proven results. A CoolSculpting session requires no needles, surgery or downtime, which makes it a great alternative to liposuction. It is ideal for candidates who have hard-to-lose-fat in areas that are resistant to exercise and diet.

"We are excited to offer this treatment option to our patients at Ederra Bella. CoolSculpting has shown significant results in removing fat, without the potential risks and downtime of invasive procedures. I have found it to be extremely effective, especially on resistant localized areas, such as back fat, love handles and isolated belly fat. The CoolSculpting procedure is quite comfortable, and patients are highly satisfied with the aesthetic outcomes," says Dr. Myla Bennett

The number of treatments required for the desired results can vary. Dr. Myla Bennett will develop a customized CoolSculpting treatment plan based on an individual's needs, the areas focused on and budget. Treatment time typically lasts between one to two hours, and patients can have additional sessions for more pronounced effects. Ederra Bella Plastic Surgery and Medical Spa's location creates a relaxed setting for patients to receive cosmetic surgical and medical spa treatments, including CoolSculpting. Dr. Myla Bennett and her team offer a wide range of procedures, such as breast augmentation, tummy tucks, liposuction, dermal fillers and injectables, anti-aging treatments and more.

More about Myla Bennett, M.D.

Dr. Myla Bennett is a well-respected, board-certified plastic surgeon and skincare expert. She earned her medical degree from the Ohio State University of Medicine and completed her plastic and reconstructive surgery and general surgery residencies there as well. She then continued her training at the university with admission to the fellowship program. With several years of experience in the industry, Dr. Myla Bennett uses her expertise to perform plastic surgery procedures and other treatments with the goal of enhancing patients' natural beauty.

For more information on CoolSculpting and other services available at Ederra Bella Plastic Surgery and Medical Spa, please call (678)-325-0006 or visit http://www.ederrabella.com.

SOURCE Ederra Bella

Original post:

Ederra Bella Plastic Surgery and Medical Spa in Johns Creek, Georgia, is Now Offering the Innovative CoolSculpting Procedure for Patients - Yahoo...

This article originally appeared on WoundReference.

Welcome to another post on plausible, off-label uses for hyperbaric oxygen therapy (HBOT). We have previously discussed the rationale for using hyperbaric oxygen therapy (HBOT) in an off-label indication. We suggested that there must be a scientific rationale, physiology that made sense for use of HBOT, and some sort of verified outcome (case report, case series, controlled clinical trial, etc.).

Today, we are going to discuss the use of HBOT for patients who have an ischemia/reperfusion injury (IRI) to the myocardium. While HBOT has been studied after acute myocardial infarction (AMI) in conjunction with stenting/angioplasty and/or alteplase (tPA) administration, our primary focus will primarily be on patients who have a planned instrumentation of the coronary arteries or coronary artery bypass grafting (CABG) surgery.

Unfortunately for you, the reader, this discussion needs to spend some time in the world of cellular and molecular biology. We will briefly discuss the effects of HBOT at the cellular and gene level within the body (primarily vascular endothelial cells).

Of necessity, the brevity of this discussion will leave a number of gaps for you to fill in. However, I will provide you with a list of reference papers to read.

Some of you took a course in cellular/molecular biology in college. I certainly did, because that was a required upper-level course for biology majors. I kept the textbook for a number of years. Whenever I would read from that textbook, I would fall soundly asleep. Now, I'm looking at a stack of cellular/molecular biology articles dealing with the heart and HBOT. After all these years, and many gray hairs ... wait for it ... wait for it ... I still fall soundly asleep.

So, I'm going to cut to the chase and give you my opinion first!

If I were scheduled to have an angioplasty/stenting or a CABG procedure, I would DEFINITELY approach the hyperbaric physician and cardiologist about having a standard wound healing HBOT table (2.4 ATA for 90 minutes of O2 breathing with standard air breaks) one time immediately (within 4 hours) before the procedure.

There are several randomized controlled studies and multiple animal models that suggest this simple, one-time, treatment reduces risk of death, preserves more myocardial tissue, reduces intensive care unit (ICU) stay, reduces overall blood loss, preserves ejection fraction, and reduces restenosis rates. While we will not discuss it, there are also hints that this one-time treatment reduces the post-cardiopulmonary bypass confusion ("pump brain") that is thought to be caused by lipid peroxidation.

Now for the details. Hold onto your hats, because we are going to move through several areas of research. I will hit only the high points and try not to overwhelm you with minutiae or too many acronyms. Fortunately, or unfortunately, you are going to see how my mind works in devious ways in order to make sense of this literature.

I performed a PUBMED search using the terms "hyperbaric oxygen" cardiac preconditioning. The results netted 17 papers, of which 11 were pertinent to this topic. As a result of searching the references within these papers, two more papers were found of pertinent interest: the HOT-PI and the HOT MI trials.

The Rubicon Foundation repository of hyperbaric oxygen studies was also queried. There were two papers that were duplicated in the PUBMED search and one abstract presented at the UHMS Annual Scientific Meeting in 2007. Of interest, this abstract was written by the same research group who published several studies found in the PUBMED collection and provides more detail.

Great questions! We will discuss the papers in chronological order. Some of the early HBOT work in this area began in 1997...

The first pilot study (HOT MI) was a randomized clinical trial composed of 82 patients and 16 were excluded for hemodynamic instability. Sixty-six were analyzed with 34 in the tissue plasminogen activator (rTPA) only group and 32 in the HBOT plus rTPA group. These patients had an acute myocardial infarction (AMI) and all were recipients of rTPA. There was no sham treatment with HBOT in this trial.

The end result of the study was that the HBOT group had lower creatine kinase (CK) levels at 12 and 24 hours. There were two deaths in the control group and none in the HBOT group (not significantly different). There was a trend to higher ejection fraction in the HBOT group (not significant). It would take nearly five years for other research groups to see this trial and begin to look at mechanisms that support HBOT in the presence of IRI of the heart. But, they did.

A 2002 randomized controlled clinical trial of patients with either unstable angina or AMI undergoing percutaneous coronary intervention (PCI) would be the next stepping stone for HBOT and cardiac preconditioning. The primary endpoints of this study were death, repeat MI, emergent CABG, and target lesion restenosis at 8 months.

To qualify for this study, the patients must either have unstable angina or an AMI. Fifty-one patients were enrolled with 24 in the HBOT arm and 27 in the control arm. There was no sham treatment to the control arm. The HBOT arm patients received two HBOT treatments consisting of 2.0 ATA for 90 minutes of oxygen breathing and no recorded air breaks. The first treatment was either 2 hours before or immediately after PCI with a second treatment within 18 hours after the first treatment.

Results were positive for HBOT preconditioning. In follow-up, 8 months from the cardiac incident and intervention, there was one repeat MI in the HBOT group and four in the control group (not statistically significant). There were five restenosis lesions in the control group and none in the HBOT group (p= 0.026). No emergent CABG in either group.

Two deaths in the control group during the 8-month follow-up period (not statistically significant). Finally, recurrence of chronic angina developed in six control patients and no HBOT patients (p=0.014). While there could be some bias caused by no sham HBOT control, this is unlikely to be a problem because the final review was 8 months following the intervention.

These authors did not measure any biochemical or other cellular markers. However, they do theorize that heat shock protein (HSP) may ameliorate oxidative stress and that lipid peroxidation was decreased. Much of the bench science of HBOT and IRI has yet to be discovered and fully tested, but this RCT again shows the positive effect of preconditioning the heart for interventional procedures. Another positive clinical study.

New technologies for mapping gene responses at cellular levels, cellular chaperones, and biochemical markers have emerged by 2006. These could only be imagined and hinted at previously. Yogaratnam (an important researcher in this sub-specialty interest) and colleagues first attempt to explain the biochemical and cellular response mechanisms for HBOT and myocardial function. In addition, they hint that there are protective oxidative functions for HBOT, reactive oxygen species (ROS), and other oxidative mechanisms.

The core mechanism for HBOT function is amelioration of the IRI. The primary fact is that an ischemic injury with resultant reperfusion sets off an inflammatory cascade at which white blood cells are called to the area of injury (the function of cellular chaperones), clog the arterioles/capillaries, degranulate, and set off a self-propagating inflammatory reaction, thus resulting in significant programmed cell death (apoptosis).

HBOT can reduce the injury and preserve tissue through reducing the ability of the WBC to attach and degranulate in the vascular endothelium. (I'm going to leave this reference to the reader, but perform a PUBMED search on the terms "Thom S" and white blood cell binding nylon columns.)

Hint: Think about Velcro. The vascular walls are the "loops" and the WBCs are the "hooks" in Velcro. When the hooks attach to the loops, then degranulation and injury occurs. Obviously, HBOT applied before or at the exact time of injury would give the best outcome (by reducing/preventing the loops to become active). But, there is a small time window (an hour or so) after injury whereby HBOT reduces the amount of myocardial injury.

Still awake? Read on ...

There are also hints that myocardial ischemia and stress activate several heat shock proteins (HSP). These are thought to have protective roles for myocardial tissues. The research question (as of 2006) is, "Does HBOT induce HSP activation?" And, the answer is a distinct "Maybe." Technology in 2006 still limits finding a definitive answer. But, technology will catch up ... you'll see.

Still with the Yogaratnam (2006) paper, we find that a number of tissues (skeletal muscle, heart muscle, small bowel, and liver) also respond positively to HBOT prior to occlusion and reperfusion injury. The tissue exposed to HBOT prior to the insult maintained homeostasis and ATP levels vs. control. In addition, this paper discusses HBOT and ROS. While we have thought about ROS after HBOT as a negative, this is not shown in the literature. In fact, the opposite has been noted.

HBOT-generated ROS are thought to decrease neutrophil adhesion by one (or more) of the following mechanisms:

The Yogaratnam (2006) paper demonstrates multiple pathways of activity for HBOT and preservation of myocardial function through a thorough evaluation of the extant literature of the day.

Their conclusion is that there are many examples of research that support HBOT in revascularization use, however those theories could not be demonstrated in the laboratory. I suspect that was simply due to lack of advanced techniques in exposing small proteins and pathways that measure in the kilo-Dalton range (very, very small proteins). The authors conclude that the use of HBOT in organ preconditioning is a fascinating theory in its infancy and bears exploring fully.

The second study by this group posits that IRI is inevitable during CABG. In this paper, they focus heavily on the research that shows HBOT to stimulate NO. This NO production may be responsible for a measurable myocardial protective effect. This paper again provides significant background material that prepares the team for human clinical research.

In 2010, the same team detailed results from a randomized, controlled, blinded clinical trial of using HBOT exposure prior to CABG. From January 2005 to July 2006, there were 774 consecutive patients presenting for first-time elective CABG. Of those patients, 81 matched the study criteria and were randomized to control (no HBOT prior) or the HBOT group (2.4 ATA for 60 minutes of O2 breathing with one 5-minute air break).

This treatment was completed approximately 4 hours prior to CABG. All other treating physicians were blinded as to study patients vs. control. The control group (unfortunately) were not treated in a sham manner, hence a small tick-off to interpretation bias potential since the researchers did know which patients received preconditioning. Note that the researchers had no input in any part of the patient surgery, postoperative care, or overall management. This is a small detriment to an otherwise excellent study!

The purpose of the RCT was to demonstrate that the effect of HBOT preconditioning was capable of improving left ventricular stroke work (LVSW). There was a clear increase in stroke volume (SV) and LVSW in the HBOT preconditioned patients. And, as icing on the cake, the HBOT preconditioned group had a number of secondary endpoints significantly different from the control group.

The HBOT group had a smaller rise in Troponin T (evidence of lesser myocardial stunning), an 18% drop in ICU length of stay (LOS), nearly 12% less blood loss, lower blood transfusion requirements, lower need for inotrope support, lower pulmonary complications (less intubated time), and lower incidence of wound infections.

From a fiscal standpoint, this group presented an abstract at the 2007 UHMS Annual Scientific Meeting. At that time, the study discussed above had been closed approximately one year and their data analysis was still ongoing. However, they showed a $570/patient savings in ICU costs to the hospital. Over the timeframe of this study (for 40 patients), the savings was nearly $20,000 (2007 USD).

At this point, I'm taking a slight jog in the course of literature review. It's about this time (2010) where laboratory science catches up and can demonstrate the effects of HBOT on tiny subcellular and biochemical markers. In particular, there are two studies by Godman, et. al. that deserve some attention.

The first study is a genome-wide microarray analysis of gene expression on human microvascular endothelial cells exposed to HBOT under the same conditions as human patients. The controls received 100% O2 and 1 ATA for the same time that the other cell culture received HBOT (2.4 ATA for 60 minutes O2 exposure).

Just for your information, this paper still puts me to sleep when I read it ... however, it is full of undeniable gene stimulation or inhibition, up-regulating six cellular chaperones, and other mind-boggling details. As a result of one HBOT exposure, there were 8,101 genes that were significantly regulated (up or down) in the HBOT group. Nearly 4,000 of these genes were still up/down regulated at measurements 24 hours after HBOT exposure.

The authors were particularly interested in the usefulness of HBOT as a preconditioning stress in order to protect cells and gene expression. Note to reader ... the following should sound familiar ... The chaperone genes are related to HSP. A number of these genes were still active 24 hours after HBOT exposure. A secondary endpoint of this research was that the microvascular cell culture exposed to HBOT immediately started to form vascular tubules vs. no differentiating growth in the control group.

Interesting, huh? Aren't you glad to be reading the condensed version?

Godman et al. published a second paper in 2010 looking at effects of HBOT and antioxidant gene expression. They found an up-regulation of antioxidant and cytoprotective effects that resisted otherwise lethal oxidative stress. While I disagree with their conclusion that HBOT may become an anti-aging wonder, the basic science in the paper makes it worthwhile reading.

Yogaratnam returns (2011) with a secondary review of their earlier data, specifically myocardial biomarkers suggesting that HBOT preconditioning induced cardioprotection following IRI. Good stuff. By now, you know this research group's methods and general results. I will simply report that they analyzed results of eNOS and HSP72 between the HBOT and control populations. In the HBOT group, both eNOS and HSP72 were increased.

Well, where are we in the grand scheme of explaining the research?

I think I've covered the bench research down to the gene level in adequate detail. All of the bench research focuses on components that show HBOT to be cytoprotective. I've discussed three randomized controlled trials with significant statistical power. These studies demonstrate HBOT effectiveness in myocardial survival and lowering serum markers showing myocardial injury patterns. What more do we need before we have enough evidence to say that this indication is plausible, even if it is off-label?

Hang on tight. More papers and more trials yet to report.

Oh, have I said it? Nope, not one negative trial up to this point. Let's see how that holds up.

A 2011 paper shows a research protocol using rat myocardium and permanent ischemia. They demonstrated that myocardial infarct size was significantly smaller in the HBOT preconditioned rats. They also showed apoptotic pathways were suppressed, resulting in preserved myocardium. They discussed a biphasic tolerance pathway against subsequent insults. The first lasted 2-3 hours after HBOT exposure, then a second, delayed, phase from 24-72 hours.

Another RCT was published in 2011 looking at cerebral and myocardial protection in patients undergoing CABG. This is a randomized, controlled, single-blinded study involving 25 control and 24 HBOT candidates. The preconditioning period was over five days prior to CABG. HBOT treatments were at 2.0 ATA with 70 minutes of oxygen breathing in two periods separated by a 5-minute air break.

The results of the study mirror those of the Yogaratnam study with similar reduction in ICU stay, reduced ventilatory ICU support, and reduced blood loss. The studies differed in hemodynamic values, and this study found no difference with PVR, SW, and LVSW after surgery.

The authors do admit that sample size in this study is small and they may not have the statistical power to notice small differences between groups. They demonstrated a reduced biomarker burden in the HBOT group for neurologic and cardiac injury. They theorize that the HBOT effects had to do with endogenous antioxidant activity being more beneficial for patients in the active HBOT group.

An entire Undersea and Hyperbaric Medicine journal (2015, Volume 2) issue is devoted to preconditioning and HBOT. The editorial for this issue laments the fact that HBOT is not routinely used prior to cardiac insult in the U.S. The treatment is simple, with few negative side effects, and relatively inexpensive.

We conclude with a Serbian study just published in 2019. This is a bench laboratory study of rat myocardium. There were 4 study groups and all study groups received HBOT. 1) HBOT only, 2) HBOT + Verapamil, 3) HBOT + amlodipine, and 4) HBOT + nicorandil.

The study involved a 20-minute global ischemia of the heart and a 30 minute reperfusion period before the animal was sacrificed. After reporting results, this study shows that all four groups were benefited from preconditioning with HBOT. In addition, the amlodipine group better preserved functional and structural properties of the heart after ischemia.

I told you at the beginning of the blog where my sympathies lie for this intervention. Nothing has changed. Every study (animal and human) demonstrated the cardioprotective effect of HBOT preconditioning prior to PCI or to CABG surgery when cardiopulmonary bypass was used. To be fair, there was one paper with several patients in the CABG group who had off-bypass surgical procedures. Cardioprotection from HBOT was less evident in that subset.

I think that there are enough studies with enough positive evidence of effect that cardioprotection with HBOT should be a UHMS-approved indication. That decision has not happened yet, although it will likely be visited in the near future.

In case you missed it, see the introduction to this blog series. This blog series focuses on conditions that are off-label and have plausible literature evidence for improvement after HBOT:

Continue reading here:

Investigational hyperbaric oxygen therapy indications: Preconditioning for cardiac surgery - MultiBriefs Exclusive