Category Archives: Anti-Aging Medicine

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

Tight Chin From Ultherapy

VANCOUVER, B.C. (PRWEB) December 12, 2019

North Americas foremost clinic in providing Ultherapy to clients and patients, as well as training doctors to administer the treatment, is based in Vancouver, Canada!

Vancouver Laser & Skin Care Centre earned the title of the official "North American Ultherapy Training Centre" from Merz Aesthetics, the creators of Ultherapy, making it the only clinic in the continent with that designation.

Ultherapy has been hailed as a revolutionary Health Canada and FDA approved treatment that uses focused ultrasound therapy to lift and tighten skin on the face and neck. It has been reviewed and praised by major publications like the New York Times, Esquire, Vanity Fair, and Elle.

Over the course of up to three hours, highly skilled technicians at the Vancouver Laser & Skin Care Centre use the clinics Ultherapy system to deliver focused ultrasound energy to the foundational layer of the skin in the targeted area in order to achieve a tightening effect without an invasive surgery.

Ultherapy is the gold standard using focused ultrasound to perform nonsurgical facial tightening and slimming, says Dr. Martin Braun, founder of Vancouver Laser & Skin Care Centre.

Unlike traditional laser, radio frequency, or surgical treatments, Ultherapy allows doctors and technicians to see the layers of tissue being targeted during the procedure, which lets them ensure that ultrasound energy is directed to where it will be most beneficial.

Ultherapy requires no recovery time for clients who may start to see their skin tightening immediately after the treatment. The body then produces more collagen deep below the skins surface during its natural healing process, giving the treated area its intended firmness and lift.

Clients who receive the treatment in various parts of their face and neck have repeatedly left rave reviews for its efficacy in essentially reversing the effects of aging.

Based on reviews submitted by over 350 Ultherapy patients in prominent plastic surgery review website, Real Patient Ratings, the process has a whopping 4.59/5 stars, earning it a 91.8% patient satisfaction rating.

I noticed that as the weeks went on, the results [from Ultherapy] just got better and better and better, said one user after receiving the treatment.

Other than its non-invasive yet effective nature, one of the most laudable aspects of Ultherapy is the fact that patients can resume normal everyday activities with no restrictions after the procedure, and its side effects are mild and temporary.

This ground-breaking treatment has been offered at the Vancouver Laser & Skin Care Centre for nearly six years and is the only non-invasive procedure approved by the FDA to lift skin on the neck, under the chin, on the eyebrow, and the dcolletage or chest area.

The Vancouver Laser & Skin Care Centre performs more Ultherapy treatments than any other clinic in Canada, earning its technicians and practitioners the ultimate trust of patients and doctors who seek to learn the procedure.

In their April 2016 issue, New Beauty magazine invited their readers to try the procedure, saying If loose skin is a problem and you need a solution, but surgery isnt an option, this skin-lifting treatment is the way to go.

Meanwhile Harpers Bazaar magazine wrote a story unboxing the contents of a gift bag after the Grammy Awards and, finding a session of Ultherapy treatment among the presents, called it almost better than the actual Grammy.

Its not difficult to see why the procedure would incite such excitement and, especially when performed by the accredited experts at the Vancouver Laser & Skin Care Centre, borders on miraculous for clients who want to match their appearance to how they feel on the inside.

About Vancouver Laser & Skin Care Centre:

A physician directed cosmetic clinic that was founded by Dr. Martin Braun and Dr. Susan Braun in 1996. With state of the art technology and a wealth of experience and knowledge, Vancouver Laser is THE non-surgical solution to all things cosmetic. In the clinics 20+ year history, their professionals have treated thousands of patients with a diverse range of conditions. Vancouver Laser has injected over 2 million units of BOTOX into patients and have honed and perfected their anti-aging strategies to provide patients with their ideal outcomes. For more information about Vancouver Laser & Skin Care Centre, visit vancouverlaser.com.

About Merz, the creators of Ultherapy:

Merz North America is a specialty healthcare company headquartered in Raleigh, North Carolina and dedicated to the development and marketing of innovative quality products for physicians and patients across the United States and Canada. Merz products are distributed through two divisions, Aesthetics and Neurosciences, and are developed with the goal of improving patients health and quality of life by delivering therapies that bring about real progress. Founded in 1908, Merz Pharma Group is a privately-owned company headquartered in Frankfurt, Germany with a global focus on aesthetic medicine and neurotoxins. For more information about Merz, visit merzusa.com.

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Researchers have identified waves of proteins in blood that peak at three distinct stages of life. What do the findings mean for aging? ER Productions Limited/Getty Images hide caption

Researchers have identified waves of proteins in blood that peak at three distinct stages of life. What do the findings mean for aging?

Scientists know that if they transfuse blood from a young mouse to an old one, then they can stave off or even reverse some signs of aging. But they don't know what in the blood is responsible for this remarkable effect.

Researchers now report that they've identified hundreds of proteins in human blood that wax and wane in surprising ways as we age. The findings could provide important clues about which substances in the blood can slow aging.

The scientists studied nearly 3,000 proteins in blood plasma that was drawn from more than 4,000 people with a span of ages from 18 to 95. The project focused on proteins that change in both men and women.

"When we went into this, we assumed you aged gradually, so we would see these changes taking place relatively steadily as individuals get older," said Tony Wyss-Coray, a professor of neurology at Stanford University.

Instead, Wyss-Coray and his colleagues report in Nature Medicine on Thursday that these proteins change in three distinct waves, the first of which happens "very surprisingly" during our 30s, peaking around age 34.

"Then we found a second wave around 60, and then we found a third one, the most prominent one, really around 80 years of age," Wyss-Coray said. (An earlier version of their paper is freely available on the bioRxiv preprint server.)

This observation raises a host of questions about the biology of aging. What age-related transition is occurring in our 30s? And what do the changes in the blood actually mean?

"Most of the proteins in the blood are actually from other tissue sources," he said. "So we can start to ask where ... these proteins come from and if they change with age," he said. For example, in proteins traced back to the liver, "that would tell us that the liver is aging."

Eventually, Wyss-Coray said, he would like to compare a patient's blood protein pattern with the pattern that's normally seen, to produce a personalized aging clock "where I can tell you, based on the composition of your blood, your kidney seems to be aging faster than it should."

Thinking back to those age-reversing experiments in mice, it might also be possible to isolate proteins in the blood that contribute to that effect.

Transfusing blood plasma carries some risks in fact, this year the Food and Drug Administration slapped down companies for trying to sell plasma from young people as an anti-aging elixir. It would be better to isolate components in the blood that are responsible for beneficial effects.

Research groups are already studying proteins one by one to find those that might actually influence health. For example, Irina Conboy's lab at the University of California, Berkeley has been studying a protein called TGF-beta, which contributes to aging. Her mouse experiments suggest that aging effects can be slowed when this protein is blocked.

Wyss-Coray founded a company, Alkahest, that's running research in people with mild to moderate Alzheimer's disease, based on the concept of infusing blood plasma to stave off disease.

With this flood of new data about blood proteins, it's a daunting task to figure out whether each one causes aging, slows it down or is merely a result of the aging process. Sorting out that question about causality is important. After all, graying hair is a biomarker of aging, but hair dye won't reverse the underlying biology.

This research "is really the first step in categorizing and cataloging the age-related biomarkers," says Toshiko Tanaka, a research scientist at the National Institute on Aging. She was the lead author on a study last year that used similar techniques and also identified many proteins related to aging. She did not look for the surprising age-related wave pattern that Wyss-Coray is now describing.

Tanaka says new technology that allows scientists to identify many proteins simultaneously is accelerating this research dramatically.

"One of the great things about these advancements in technology is it's becoming a lot cheaper to measure a lot of these molecules," she says, "so bigger studies and more studies can assess the same proteins."

That means discoveries in one lab can be validated elsewhere. But it's also the case that there is a vast sea of blood proteins and other constituents yet to explore, any of which may be involved in health and disease.

"For a long time we have focused, in the field of healthy aging, on genetics," says Paola Sebastiani, a biostatistics professor at Boston University who has also researched the link between aging and proteins in the blood.

But your genes are set from birth, and they can't be modified to improve your health. What's intriguing about blood proteins and similar molecules is that you can block them or find other ways to modify them with drugs, at least in theory, "until eventually you're going to help people age healthily," she says.

Tanaka isn't expecting quick answers from this line of research, but "I hope by the time my kids are old, this is something that can help improve their health's trajectory."

You can contact NPR science correspondent Richard Harris at rharris@npr.org.

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Assessment of the Anti-Aging Medicine Market

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Anti-Aging Medicine Market is set to reach a value of ~US$ XX Mn/Bn by the end of 2018 - 2026 - The Market Expedition

PASADENA, Calif., Dec. 6, 2019 /PRNewswire-PRWeb/ --Maria Sulindro-Ma, M.D.'s book The No Coat Medicine: A Guide for Living a Long and Healthy Life ($24.99, paperback, 9781545676394; $42.99, dust-jacket, 9781545660317; $2.99, e-book, 9781545661284), is available for purchase.

The No Coat Medicine: A Guide for Living a Long and Healthy Life gives readers simplified tipes to stay healthy and feel young. With these Six Pillars, readers will learn to watch what they should not have to help detox, avoid what causes inflammation, keep moving, be happy, and balance their hormones.

As a pioneer in Anti-Aging Medicine, Maria Sulindro-Ma, M.D. is often asked if she does facial rejuvenation and she always answers carefully that she does the whole-body internal rejuvenation without surgery or drugs. They are interested in modern medicine where we do not just depend on surgery, drugs, or food, but we depend on preventive measure by changing our lifestyle and the way we anticipate health stage over the sickness.

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Readers Can Learn to Improve Their Health by Changing Their Lifestyle - Benzinga

Dr. Alexis Parker, MD Gives Five Units of Botox to Patients Who Bring in Toys During the Holidays

DENVER (PRWEB) December 06, 2019

Lasair Aesthetic Health Sponsors Toys for Tots to Give Free Toys to Children in Need

Dr. Alexis Parker, MD Gives Five Units of Botox to Patients Who Bring in Toys During the Holidays

Lasair Aesthetic Health is spreading holiday cheer again this year by sponsoring the Toys for Tots program. From now until Christmas, patients who bring in a toy or toys worth more than 25-dollars, will get FIVE units of Botox (a $60 value) for free from Lasair.

Dr. Alexis Parker, MD and her staff at Lasair Aesthetic Health have donated hundreds of toys to the Toys for Tots Program over the past decade. They are thrilled to once again accept donations and take another sleigh full of toys (a.k.a. a mini-van) for the Marine Toys for Tots donation center. "I feel so lucky to have such wonderful patients with caring hearts who donate toys for those who are less fortunate in our community," Dr. Parker said.

The Toys for Tots program has collected and distributed toys to children in need for nearly 70-years to help children throughout the United States to experience the joy of Christmas. The Marine Toys for Tots Program collected and distributed 18-million toys to seven million less fortunate children over this past year.

Dr. Alexis Parker, M.D. is board certified by the American Academy of Anti-Aging and Regenerative Medicine and has been labeled one of Denver's top non-surgical aesthetic physicians. Dr. Parker trained in general surgery and plastic surgery, and subsequently boarded in emergency medicine. She also did a 6 month fellowship in the plastic surgery department at UC Irvine. After 16 years in the Emergency Department, she turned back to her true passion: helping people look and feel their best, non surgically, using the latest in non-invasive cosmetic dermatology procedures which include laser technology, injecting techniques, and home skin care.

CONTACT: Jesse Luginbuhl (303) 782-5082

6780 E Hampden Avenue Denver, CO 80224

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