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Will Smoking Pot Harm Your Heart? Experts Weigh In

Will Smoking Pot Harm Your Heart? Experts Weigh In

News Picture: Will Smoking Pot Harm Your Heart? Experts Weigh InBy Dennis Thompson
HealthDay Reporter

MONDAY, Jan. 22, 2018 (HealthDay News) — Anyone worried that smoking a lot of pot could lead to a heart attack or stroke will just have to keep worrying for the time being.

There’s not enough scientific evidence to say one way or the other how marijuana affects heart health, a new review has concluded.

“Our review found insufficient evidence to draw meaningful conclusions that marijuana use is associated with cardiovascular risk factors and outcomes,” said lead study author Dr. Divya Ravi, an internist with the Wright Center for Graduate Medical Education in Scranton, Pa.

For their review, Ravi and her colleagues pored through medical literature and found 24 studies that evaluated marijuana use and its effects on either heart health risk factors or actual health problems such as heart attack or stroke.

A few studies showed that pot use might benefit the heart, but these were contradicted by other studies that reported potential harmful effects, Ravi said.

For example, some studies linked marijuana use to less diabetes, lower blood sugar and higher levels of “good” HDL cholesterol, the researchers found. And despite anecdotal reports of marijuana bringing on the “munchies,” no studies have tied pot use to weight gainor obesity.

However, other studies found that smoking pot was associated with a greater risk for heart attack and death from heart disease.

“The evidence is insufficient to draw any conclusions,” Ravi said. “The association between marijuana and cardiovascular health has not been adequately studied to date.”

Two heart experts not involved with the study said they’re not surprised by the lack of evidence, given how difficult it is to conduct studies on marijuana use.

Results could become more definitive in the future, thanks to some states legalizing marijuana. That might make people more comfortable discussing their pot use with researchers, said Dr. Russell Luepker, a professor with the University of Minnesota’s School of Public Health.

The vast majority of states allow limited use of medical marijuana under certain circumstances. And eight states and Washington D.C. have legalized recreational pot use.

Dr. Satjit Bhusri, a cardiologist at Lenox Hill Hospital in New York City, said it’s very likely that smoking pot can harm heart health because you’re actively breathing in smoke.

“If you inhale a joint it’s like inhaling a cigarette — you’re putting toxins in your body,” Bhusri said.

On the other hand, it’s hard to say that eating or vaping marijuana produces the same heart risk, said Luepker, a spokesman for the American Heart Association.

“Like any smoked product, you inhale a variety of things, including carbon monoxide and other substances that you certainly don’t get if you eat it,” Luepker said.

Bhusri also expects that the more someone smokes pot, the more they’d increase their heart health risk.

“I wouldn’t be surprised if there is a dose relationship because of these toxins that are inhaled,” he said.

But because marijuana users don’t smoke at the same rate as those who smoke cigarettes, Luepker said, it’s not likely they will be doing themselves as much harm.

For instance, it’s hard to think of many people smoking two packs a day of pot, or lighting up first thing in the morning, he said.

Marijuana users are more akin to “social cigarette smokers who smoke a cigarette or two at a party, and they don’t seem to have any increased risk from that,” Luepker said.

Until more is known, though, pot users should use caution, Ravi concluded.

“At this juncture we have little data on potential harms or benefits associated with use to inform the counseling of marijuana users,” Ravi said. “It may be wise to proceed with caution until we have sufficient evidence to comment on the health effects of chronic marijuana use.”

The study is published in the Jan. 23 issue of Annals of Internal Medicine.

Early warning signs for kidney and heart disease

Signs and symptoms of chronic kidney disease develop over time if kidney damage progresses slowly. Signs and symptoms of kidney disease may include:

  • Nausea
  • Vomiting
  • Loss of appetite
  • Fatigue and weakness
  • Sleep problems
  • Changes in how much you urinate
  • Decreased mental sharpness
  • Muscle twitches and cramps
  • Swelling of feet and ankles
  • Persistent itching
  • Chest pain, if fluid builds up around the lining of the heart
  • Shortness of breath, if fluid builds up in the lungs
  • High blood pressure (hypertension) that’s difficult to control

Signs and symptoms of kidney disease are often nonspecific, meaning they can also be caused by other illnesses. Because your kidneys are highly adaptable and able to compensate for lost function, signs and symptoms may not appear until irreversible damage has occurred.

Simple EKG Can Determine Whether Patient Has Depression or Bipolar Disorder

Simple EKG Can Determine Whether Patient Has Depression or Bipolar Disorder

Summary: Heart rate variability can indicate whether a person has bipolar disorder or major depression, a new study reports.

Source: Loyola University Health System.

A groundbreaking Loyola Medicine study suggests that a simple 15-minute electrocardiogram could help a physician determine whether a patient has major depression or bipolar disorder.

Bipolar disorder often is misdiagnosed as major depression. But while the symptoms of the depressive phase of bipolar disorder are similar to that of major depression, the treatments are different and often challenging for the physician.

In bipolar disorder, formerly called manic depression, a patient swings between an emotional high (manic episode) and severe depression. Treatment for the depressed phase includes an antidepressant along with a safeguard such as a mood stabilizer or antipsychotic drug to prevent a switch to a manic episode. A physician who misdiagnoses bipolar disorder as major depression could inadvertently trigger a manic episode by prescribing an antidepressant without a safeguard mood stabilizing drug.

The study found that heart rate variability, as measured by an electrocardiogram, indicated whether subjects had major depression or bipolar disorder. (Heart rate variability is a variation in the time interval between heartbeats.) The study, by senior author Angelos Halaris, MD, PhD and colleagues, was published in the World Journal of Biological Psychiatry.

“Having a noninvasive, easy-to-use and affordable test to differentiate between major depression and bipolar disorder would be a major breakthrough in both psychiatric and primary care practices,” Dr. Halaris said. Dr. Halaris said further research is needed to confirm the study’s findings and determine their clinical significance.

Dr. Halaris is a professor in Loyola’s department of psychiatry and behavioral neurosciences and medical director of adult psychiatry.

Major depression is among the most common and severe health problems in the world. In the United States, at least 8 to 10 percent of the population suffers from major depression at any given time. While less common than major depression, bipolar disorder is a significant mental health problem, affecting an estimated 50 million people worldwide.

The Loyola study enrolled 64 adults with major depression and 37 adults with bipolar disorder. All subjects underwent electrocardiograms at the start of the study. Each participant rested comfortably on an exam table while a three-lead electrocardiogram was attached to the chest. After the patient rested for 15 minutes, the electrocardiographic data were collected for 15 minutes.

Using a special software package, researchers converted the electrocardiographic data into the components of heart rate variability. These data were further corrected with specialized software programs developed by study co-author Stephen W. Porges, PhD, of Indiana University’s Kinsey Institute.

In measuring heart rate variability, researchers computed what is known to cardiologists as respiratory sinus arrhythmia (RSA). At the baseline (beginning of the study), the subjects with major depression had significantly higher RSA than those with bipolar disorder.

In a secondary finding, researchers found that patients with bipolar disorder had higher blood levels of inflammation biomarkers than patients with major depression. Inflammation occurs when the immune system revs up in response to a stressful condition such as bipolar disorder.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

The study is titled “Low cardiac vagal tone index by heart rate variability differentiates bipolar from major depression.” In addition to Drs. Halaris and Porges, other co-authors are Brandon Hage, MD, a graduate of Loyola University Chicago Stritch School of Medicine now at the University of Pittsburgh (first author); Stritch student Briana Britton; Loyola psychiatric resident David Daniels, MD; and Keri Heilman, PhD of the University of North Carolina.

Source: Jim Ritter – Loyola University Health System
Publisher: Organized by NeuroscienceNews.com.
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Abstract for “Distinguishing bipolar II depression from unipolar major depressive disorder: Differences in heart rate variability” by Hsin-An Chang Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Chuan-Chia Chang, Terry B. J. Kuo & San-Yuan Huang in World Journal of Biological Psychiatry. Published online November 14 2017 doi:10.3109/15622975.2015.1017606

Loyola University Health System “Simple EKG Can Determine Whether Patient Has Depression or Bipolar Disorder.” NeuroscienceNews. NeuroscienceNews, 20 November 2017.
<http://neurosciencenews.com/ekg-depression-bipolar-7991/&gt;.

Abstract

Distinguishing bipolar II depression from unipolar major depressive disorder: Differences in heart rate variability

Objectives. Bipolar II (BPII) depression is commonly misdiagnosed as unipolar depression (UD); however, an objective and reliable tool to differentiate between these disorders is lacking. Whether cardiac autonomic function can be used as a biomarker to distinguish BPII from UD is unknown.

Methods. We recruited 116 and 591 physically healthy patients with BPII depression and UD, respectively, and 421 healthy volunteers aged 20–65 years. Interviewer and self-reported measures of depression/anxiety severity were obtained. Cardiac autonomic function was evaluated by heart rate variability (HRV) and frequency-domain indices of HRV.

Results. Patients with BPII depression exhibited significantly lower mean R–R intervals, variance (total HRV), low frequency (LF)-HRV, and high frequency (HF)-HRV but higher LF/HF ratio compared to those with UD. The significant differences remained after adjusting for age. Compared to the controls, the patients with BPII depression showed cardiac sympathetic excitation with reciprocal vagal impairment, whereas the UD patients showed only vagal impairment. Depression severity independently contributed to decreased HRV and vagal tone in both the patients with BPII depression and UD, but increased sympathetic tone only in those with BPII depression.

Conclusions. HRV may aid in the differential diagnosis of BPII depression and UD as an adjunct to diagnostic interviews.

“Distinguishing bipolar II depression from unipolar major depressive disorder: Differences in heart rate variability” by Hsin-An Chang Department of Psychiatry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, Chuan-Chia Chang, Terry B. J. Kuo & San-Yuan Huang in World Journal of Biological Psychiatry. Published online November 14 2017 doi:10.3109/15622975.2015.1017606

Thymosin beta 4 and Skin Repair

 Thymosin beta 4 and Skin Repair

By Carmia Borek, Ph.D.

IMAGE TAG

The promise of repairing sun parched aging skin is alluring, especially if damage control may be attained by applying a substance that is abundant in our body. Thymosin beta 4 (Tb4), a molecule that accelerates wound healing in animals and cultured cells, “may be valuable in repairing skin damage caused by sun or even by the wear and tear of aging?”

This hopeful message of Tb4’s potential to restore damaged human skin was voiced at the 5th International Symposium on Aging Skin, in California (May 2001), by Dr. Allan Goldstein, Chairman of the Biochemistry Department at George Washington University and founder of RegeneRX Biopharmaceuticals. RegeneRX is carrying out preclinical research on Tb4 as a wound healer, in collaboration with scientists at the National Institutes of Health.

Skin is the largest organ of the body, which makes up 16% of total body weight. It is also the largest organ that provides immune protection and plays a role in inflammation. Composed of specialized epithelial and connective tissue cells, skin is our major interface with the environment, a shield from the outside world and a means of interacting with it. As such, the skin is subjected to insults and injuries: burns from the sun’s ultraviolet radiation that elicit inflammatory reactions, damage from environmental pollutants and wear and tear that comes with aging.

Image with Caption

An effective healer, Tb4 can be
administered topically on the
surface of cells and systemically,
through injection. Besides
healing skin wounds, Tb4 has
been shown to promote repair
in the cornea of the eye, in rats,
thus preventing loss of vision.

There are several layers in the skin; the outer epidermis and beneath it the dermis and the subcutaneous layer. Cells in the epidermis include keratinocytes, its major cell type, that move continuously from the lower basal layer where they are formed by cell division. Other cells in the epidermis are the melanocytes that synthesize pigment and transfer it to the keratinocytes, giving our skin its color, and a wide variety of immune cells that maintain immune surveillance and secrete substances called cytokines, like interleukin 1 and 2, which are active in inflammation. The dermis contains connective tissue, mainly collagen, blood vessels, various types of immune white cells and fibroblasts.

The structure that provides the cell with form is the cytoskeleton, whose protein actin, a housekeeping molecule in cells, comprises 10% of the cell protein. Actin is essential for cell division, cell movement, phagocytosis (engulfing foreign bodies in immunoprotection) and differentiation.

Cells on the surface of the skin are constantly being replaced by regeneration from below. The repair of a wound is a scaling up of this normal process, with additional complex interactions among cells, formation of new blood vessels, collagen, more extensive cell division and cell migration, as well as strict control of inflammatory cells and the cytokines they release to resolve the inflammation.

Skin damage and aging are induced to a large extent by free radicals from the sun and environmental pollutants and from oxidants produced during infection and inflammation. Lipid peroxidation of membranes and increased inflammatory substances, such as thromboxanes and leukotriens, add insult to injury. While skin damage accumulates with age, repair processes slow down. Thus, any boost by a molecule that would reduce free radicals and accelerate molecular events in healing has the potential to hasten skin repair. Tb4 has such healing qualities.

The nature of Tb4

Image with Caption

The promise of repairing sun
parched aging skin is alluring,
especially if damage control
may be attained by applying
a substance that is abundant
in our body.

Thymosin beta 4 is a small 43 amino acid protein (a peptide) that was originally identified in calf thymus, an organ that is central in the development of immunity. Tb4 was later found in all cells except red blood cells. It is highest in blood platelets that are the first to enter injured areas, in wound healing. Tb4 is also detected outside cells, in blood plasma and in wound and blister fluids.

Its unique potential as a healing substance lies in that it interacts with cellular actin and regulates its activity. Tb4 prevents actin from assembling (polymerizing) to form filaments but supplies a pool of actin monomers (unpolymerized actin) when a cell needs filaments for its activity. A cell cannot divide if actin is polymerized. Tb4 therefore serves in vivo to maintain a reservoir of unpolymerized actin that will be put to use when cells divide, move and differentiate.

Tb4 has other effects that are needed in healing and repair of damaged tissue. It is a chemo-attractant for cells, stimulates new blood vessel growth (angiogenesis), downregulates cytokines and reduces inflammation, thus protecting newly formed tissue from damaging inflammatory events. Tb4 has been shown to reduce free radical levels (with similar efficiency as superoxide dismutase), decrease lipid peroxidation, inhibit interleukin 1 and other cytokines, and decrease inflammatory thromboxane (TxB2) and prostaglandin (PGF2 alpha).

An effective healer, Tb4 can be administered topically on the surface of cells and systemically, through injection. Besides healing skin wounds, Tb4 has been shown to promote repair in the cornea of the eye, in rats, thus preventing loss of vision.

Wound healing

A critical step in wound healing is angiogenesis. New vessels are needed to supply nutrients and oxygen to the cells involved in repair, to remove toxic materials and debris of dead cells and generate optimal conditions for new tissue formation. Another important step is the directional migration of cells into the injured area, joining up to repair the wound. This requires an attractant that will direct the cells to the wound and propel them to the site. These critical steps in wound healing are regulated by beta 4, as seen in the following experiments.

Endothelial cells

Cells that line blood vessels (endothelial cells), taken from human umbilical chord veins, were grown in culture and the layer of cells subjected to a scratch wound. Cultures were then treated with Tb4 or kept in growth medium without Tb4. When examined four hours later, Tb4 treatment attracted cells to migrate into the wound and accelerated their movement, showing it is a chemoattractant. Cell migration was four to six times faster in the presence of Tb4 compared to the migration of untreated cells. Tb4 also hastened wound closure and increased the production of enzymes, called metalloproteases, that could pave the way for angiogenesis by breaking down barrier membranes and facilitating the invasion of new cells to the needy area, to form new vessels. Other experiments showed Tb4 acts in vivo. When endothelial cells were implanted under the skin in a gel supplemented with Tb4, the cells formed vessel-like structures containing red blood cells, indicating the ability to stimulate angiogenesis in the animals.

Skin repair

Thymosin beta 4 accelerated skin wound healing in a rat model of a full thickness wound where the epithelial layer was destroyed. When Tb4 was applied topically to the wound or injected into the animal, epithelial layer restoration in the wound was increased 42% by day four and 61% by day seven, after treatment, compared to untreated. Furthermore, Tb4 stimulated collagen deposition in the wound and angiogenesis. Tb4 accelerated keratinocyte migration, resulting in the wound contracting by more than 11%, compared to untreated wounds, to close the skin gap in the wound. An analysis of skin sections (histological observations) showed that the Tb4 treated wounds healed faster than the untreated. Proof of accelerated cell migration was also seen in vitro, where Tb4 increased keratinocyte migration two to three fold, within four to five hours after treatment, compared to untreated keratinocytes.

Repair of the cornea

IMAGE TAG

The cornea is the outer thin layer of epithelial cells protecting the eye. After wounding, timely resurfacing of the cornea with new cells is critical, to prevent loss of normal function and loss of vision. Corneal epithelial healing occurs in stages, with cells migrating, dividing and differentiating. Therapies for corneal injury are limited. Therefore, the recent finding that Tb4 promotes corneal wound repair in animal models offers hope for a therapeutic product that will improve the clinical outcome of patients with injured corneas.

In the experiments, an epithelial wound was made in the corneas of sedated rats. A Tb4 solution was applied at several concentrations to the injured eyes in one group of rats while another group was treated with a solution without Tb4. Following 12, 24 and 36 hours, the eyes were tested by microscopic observation for epithelial growth over the injured site. Investigators found the Tb4 accelerated corneal wound repair at doses of Tb4 similar to those found to repair skin wounds. When tested 24 hours after treatment, the rate of accelerated repair was proportional to the concentration of Tb4, with the highest dose (25 microgram) showing a threefold acceleration of epithelial cell migration, compared to untreated. Treatment with Tb4 showed anti-inflammatory effects, helping resolve the injury. An application to human cells in a model of human corneal cells in culture showed that Tb4 enhanced epithelial cell migration in vitro.

RegeRx and Tb4

Thymosin beta 4, developed by RegeneRx Biopharmaceuticals as a pharmaceutical for the healing of wounds, is a synthetic version of the natural peptide. As Dr. Allan Goldstein emphasizes, “Tb4 represents a new class of wound healing compounds. It is not a growth factor or cytokine, but rather exhibits a number of physiological properties which include the ability to sequester and regulate actin, its potent chemotactic properties. . . and its capability to downregulate a number of inflammatory cytokines that are present in chronic wounds.” When a wound heals there are many growth factors produced in the area so that additional factors, such as those currently on the market for wound healing, may help but are not necessarily lacking. Tb4 treatment, however, adds a new dimension to wound repair by providing cells with actin as needed, for cell migration, replication and differentiation.

RegeneRX Biopharmaceuticals is focusing on the commercialization of Tb4 “For the treatment of injured tissue and non-healing wounds, to enable more rapid repair and/or tissue regeneration.” Especially needy are diabetics who suffer from poor blood circulation and loss of sensation of pain that keeps their wounds unnoticed and unattended for days, leading to ulcers that may not heal. Other hard healing wounds are pressure ulcers in patients who are bed ridden and often receive skin grafts as treatment, or reconstructive surgery.

RegeneRx is continuing with pre-clinical research, in collaborative arrangements with the National Institutes of Health, accumulating data on the effects of Tb4 and aiming for an IND application (Investigational New drug App-lication) to proceed with clinical studies. Phase I clinical trials will determine the ability of Tb4 to repair ulcers in diabetic patients and to reduce inflammation and accelerate recovery from burns and abrasions to the cornea.

Aging skin

IMAGE TAG

The potential of Tb4 to repair sun damaged and aging skin is yet to be established by extensive studies. Many of the biological events that occur in wounding are involved in skin impaired by sun and aging. Ultraviolet radiation damage or other injuries to skin that are associated with aging may be in the future repairable with Tb4, similar to the success with wound repair. It is a hopeful prediction that this small anti-inflammatory molecule, which plays a vital role in regeneration, remodeling and healing of damaged tissues, would help rejuvenate aging skin. The effects of Tb4 in accelerating wound repair are important following surgery; Tb4 would then have practical applications following cosmetic surgery, a procedure growing in popularity in our society, in dealing with aging skin.

References

Goldstein AL. Thymosin In: McGraw Hill Yearbook of Science & Technology, McGraw Hill Publishers, New York PP371-373.

Low T, Goldstein AL. Chemical characterization of thymosin beta 4, J Biol Chem 1982; 257:1000-1006.

Malinda KM, Goldstein AL. Kleinman HK Thymosine beta 4 stimulates directional migration of human umbilical vein endothelial cells. FASEB J 1997; 11: 474-481.

Malinda M et al. Thymosin beta 4 accelerates wound healing J Inves Dermatol 1999; 113: 364-368.

Nachmias VT et al. Thymosin beta 4 (Tbeta4)in activated platelets Eur J. Cell Biol 1993; 61:314-320.

Sanders MC, Goldstein AL, Wang YL. Thymosin beta 4 (Fx peptide) is a potent regulator of actin polymerization in living cells Proc Nat Acad Sci 1992;89:4678-4682.

Sosne G et al. Thymosin beta 4 promotes wound healing and modulates inflammatory mediators in vivo Exp Eye Res 2001; 72:605-609.

Young JD et al. Thymosin beta 4 sulfoxide is an anti-inflammatory agent generated by monocytes in the presence of glucocorticoids Nat.Med 1999;5:1424-1427.

130/80 new guideline for blood pressure – causes of high BP

The latest medical evidence has proven that people with blood pressure in the 130-139 range carry a doubled risk of heart attackstroke, heart failure and kidney failure, compared to those with lower blood pressure, said Dr. Joaquin Cigarroa, a member of the clinical guidelines task force.

There are many causes of a high BP such as trans fat, lack of sleep, carbon monoxide poisoning, metal toxicity, mold toxicity, medications and drugs, genetics, foods and other unknowns. When a person is dying, the BP is the lowest.

Trans fat foods

No more trans fats to raise blood pressure! The decision by the FDA to ban trans fats that raise blood pressure and increase risk for heart attack and stroke, is a great victory for heart health.

Sleep and blood pressure

Over time, a lack of sleep could hurt your body’s ability to regulate stress hormones, leading to high blood pressureSleeping seven to eight hours a night may play a role in the treatment and prevention of high blood pressure.

Carbon monoxide poisoning

Carbon monoxide poisoning often causes a victim’s blood pressure to rise.

Mold Toxicity

A conglomeration of dysfunction can set the stage for mold toxicity such as migraine headaches, elevated blood pressure and chronic recurrent infections.

Metal toxicity

Selenium antagonizes mercury toxicity. … Mercury, cadmium, and other heavymetals inactivate COMT, which increases serum and urinary epinephrine, norepinephrine, and dopamine. This effect will increase blood pressure and may be a clinical clue to heavy metal toxicity.

Medications and drugs

Certain pain and anti-inflammatory medications can cause you to retain water, creating kidney problems and increasing your blood pressure. Examples include: Indomethacin (Indocin, others) Nonsteroidal anti-inflammatory drugs (NSAIDs), including naproxen sodium (Aleve, Anaprox) and ibuprofen (Advil, Motrin IB, others)

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