The Benefits of Deer Antler Velvet IGF-1

Improving muscle building

• Increases proliferation and growth of muscle cells
  without a corresponding rise in fat tissue
• Increases uptake of amino acids into muscle cells, helping to regenerate muscle tissue after exercise and assure that muscle protein synthesis takes place
• Increases uptake of glucose into muscle cells
• Improves utilization of fat for energy
• Decreases utilization of carbohydrates
• Reduces catabolism (muscle break down) after training and workouts

Increasing human metabolism

• Improves white blood cell production
• Restores the immune-promoting lymphoid tissue
• Stimulates the proliferation of both B and T lymphocytes that help to kill viruses
• Increases the uptake and degradation of dangerous LDL cholesterol by macrophages
• Improves nitrogen retention (muscle preservation) and increase sodium excretion
• Improves parathyroid function vitamin D interaction to produce a dense bone matrix
• Reduces the urinary hydroxyproline excretion

Losing fat

One of the major issues with losing weight and restricting calorie intake is the accompanying loss in muscle mass. Muscle mass has been directly proven to stimulate metabolism and fat loss. Studies have shown that individuals receiving human growth hormone experience a significant lipolysis effect. Growth hormone increases the fat burning mechanism intrinsic to IGF-1; therefore, preserving and increasing lean body mass. IGF-1 also reduces cortisol levels and improves and regulates hormonal levels, which can be affected by calorie-restricted diets.

Improving the preservation of muscle mass when fat loss is experienced also benefits the health of an individual during weight loss procedures. Studies have shown that the pituitary gland contains the same amount of growth hormone through an individual’s lifetime. With age, however, the ability to release that growth hormone is blocked in the feedback loop between IGF-1 in the liver and the hypothalamus in the brain. Instead of reduced levels of IGF-1 signaling to the brain to direct the pituitary gland to make more growth hormone, this feedback loop is broken down with age. This is why supplementing with IGF-1 is not associated with a negative feedback loop.

Refer to references 34-­35.

Slowing the aging process

Growth hormone is the primary hormone of the endocrine system. As it pulsates out from the pituitary gland, it is quickly converted by the liver into IGF-1, the metabolite form of the hormone that is ready to be used by the body. Growth hormone and IGF-1 levels decrease significantly as humans get older, especially after the age of 40. The decline in growth hormone is directly associated with certain aging signs like wrinkling skin, graying hair, decreased energy, decreased sexual function, increased body fat, heart disease, and weak and brittle bones. All of these symptoms of aging can be slowed down and even reversed with administering natural IGF-1 to counteract the biological aging process.

In addition, research has shown that IGF-1 reverses the shrinking of the thymus, which is one of the most important immune modulation organs in the body. This research shows exciting benefits of IGF-1 for those looking to halt and reverse the aging process.

Refer to references 36-­38.

Increasing lifespan

IGF-1 has the potential to increase lifespan. The blueprint of life that determines age is DNA. The Department of Clinical Research at the Longevity Institute International has studied how natural sources of IGF-1 may soon be able to turn old cells into new ones. IGF-1 can help produce new healthy cells and keep them in a healthy state for as long as possible. The cells ability to function relies on the genetic material of DNA. This resides in the nucleus of the cell that codes for all proteins, hormones and enzymes that make the cell run. Oxygen radicals and other factors such as UV light are constantly damaging DNA. DNA has the ability to repair itself but this ability is dramatically reduced within the aging process. Certain antioxidants can reduce the damage to DNA, but none have been shown to be as effective as IGF-1.

European researchers have shown that IGF-1 is capable of doing what other antioxidants cannot; IGF-1 initiates the transportation of nucleic acids into the nucleus of the cell where DNA resides. It provides the raw materials necessary to repair damage to DNA and initiate cell division, helping to slow the aging process.

Refer to references 39-­40.

Improving blood sugar utilization

Synthetic human growth hormone injections can cause insulin resistance and further complicate the conditions of type II diabetics. On the other hand, natural IGF-1 actually has similar properties to insulin and helps improve the blood sugar profiles in these individuals. Studies were conducted by researchers at the Nemours Children’s Clinic in Jacksonville, Florida, on three groups of individuals with insulin resistance. They concluded that patients treated with IGF-1 had less muscle loss, improved outcomes from surgery and normalized blood sugar levels, even when administered with conflicting pharmaceuticals that are known to cause insulin resistance.

Refer to reference 41-­42.

Diabetic neuropathy

Peripheral neuropathy is a debilitating nervous system complication experienced by both type I and type II diabetics. IGF-1 expression in tissue is impaired by diabetic conditions leading to sensory and motor neuron damage. Studies have shown that restoring serum IGF-1 levels can improve motor neuron function and prevent nerve demyelization. These findings have shown that the restoration of IGF-1 levels may be an effective treatment for diabetic neuropathy.

Refer to references 43-­44.

Improving heart functions

IGF-1 has been shown to improve the cardiac functions of patients with congestive heart failure. In a randomized double-blind study conducted at the University Hospital of Zurich, the administration of IGF-1 to patients was associated with a 27% rise in the cardiac index and a 21% boost in the stroke volume index. The heart improved in strength and pumped more blood. This was also accompanied by a reduction in systemic vascular resistance, a 25% decline in pulmonary artery pressure and a 33% decrease in the right arterial pressure, while the placebo group experienced no such improvements.

Refer to references 45-­46.

Repairing nerve damage

IGF-1 has been shown to repair and reconnect severed nerve endings up to a distance of six millimeters. According to scientists at the Institute of Neurobiology at the University of Gothenburg, IGF-1 by itself or in combination with other growth factors can stimulate nerve regeneration. IGF-1 has been shown to have a remarkable growth effect on spinal cord motor neurons by increasing neural activity in the spinal culture by 150-270%. It has also been shown to significantly decrease the preprogrammed cell death in embryos and has shown a tenfold increase on the intramuscular nerve sprouting in laboratory mice.

Researchers at the University of Michigan have also demonstrated that IGF-1 can stimulate the protective covering around the nerves, the myelin sheath. In debilitating diseases like multiple sclerosis and ALS (Lou Gehrig’s disease), damage around the myelin sheath prevents signals between the brain and the nerves from being transmitted. IGF-1 and other growth factors have been shown to re-grow this protective sheath. IGF-1 was the most effective of the growth factors in inducing the growth of the myelin sheath and neuron cell and also helps the nerves remain normal and re-grow even when diabetic conditions were present.

The results of these studies are tremendous for individuals with MS and ALS who experience a loss of cortical motor neurons and for victims of other diseases that affect the peripheral nerves.

Refer to references 47-­48.

Relieving fibromyalgia

Individuals with fibromyalgia are growth hormone and IGF-1 deficient. They experience muscle weakness, a reduced exercise capacity and chronic fatigue syndrome. A recent study found that 40% of fibromyalgia patients had lower IGF-1 levels when compared to normally healthy adults in their age and gender group. The study then looked at fifty of these same individuals and found that over 82% of them lacked the ability to properly secrete growth hormone.

Research has shown that IGF-1, the metabolite of growth hormone, can improve muscular endurance, strength and immune response. Directly administering a natural IGF-1 substitute in lieu of this lack of proper growth hormone secretion could prove to be an ideal natural alternative for individuals suffering from fibromyalgia.

Refer to references 49-­50.

Reducing prostate-specific antigens

In a study conducted at the Medical College of Wisconsin, IGF-1 levels were found to be unassociated with heightened prostate specific antigen (PSA) levels. The findings, published in the International Journal of Anti-Aging Medicine, indicate that prostate cancer incidences rise as men increase in age, whereas the blood levels of IGF-1 significantly decrease over the same timeframe at a rate of about 14% per decade after the age of thirty. In fact, IGF-1 may reduce PSA readings that are greater than four. The study also found that in over 3,000 patients, no increase in prostate cancer or any other malignancy was found in long-term treatment.

In another study, Dr. Ronald Klatz, President of the American Academy of Anti-Aging Medicine, found that there were no reported cases of cancer among 800 treated patients, demonstrating that increased IGF-1 levels may have a protective and stimulating effect on the immune system. Further studies have shown that alternative therapies in treating prostate cancer with direct supplementation of endocrine hormones have actually significantly reduced PSA levels above fifty down to normal ranges of zero to four. This is attributed to the natural production of killer immune cells that were able to destroy the cancer cells.

Refer to reference 51-­52.

Improving immune system responses

There is an interesting relationship between IGF-1 and the immune system. The activity between all major immune cell types such as T-cells, B-cells, natural killer cells and macrophages is altered with increased IGF-1 levels. This is because increased IGF-1 levels are involved in the production of lymphocytes, and in turn, can actually produce more IGF-1. This provides an alternate source of IGF-1 production other than the liver and a baseline for cellular communication between the immune system and the neuro-endocrine system.

Refer to references 53-­54.

Bone fracture, density and osteoporosis

Bone related complications and illness are one of the leading concerns of the aging population today. Bone is a dynamic tissue that is constantly reabsorbing and renewing itself by principal cells that mediate this process. The three main cells involved are osteoblasts, osteoclasts, and osteocytes. IGF-1 plays a critical role in bone growth, bone mass and strength by stimulating the production and function of these cells. Studies have consistently shown that IGF-1 may have an implication in treating bone fractures and bone complications like osteoporosis.

Refer to references 55-­57.

Arthritic complications

In spite of IGF-1 expression being increased in patients with osteoarthritis and rheumatoid arthritis, there may actually be less bioavailability of IGF-1 in the body’s tissues. This is linked to the increased expression of insulin-like growth factor – binding protein (IGFBP), especially IGFBP-3 & 5, which may limit the bioavailability and affect IGF-1 has as an anabolic, anti-inflammatory, and tissue regenerating mechanism. Furthermore there is some exciting research on IGF-1 suspended in topical carriers increasing cartilage and subchondral bone repair in osteoarthritis. On the other hand patients with chronic arthritic conditions have been shown to not only have a decreased expression of IGF-1, but also a decreased expression of other hormones like growth hormone and testosterone as well.

Refer to references 58-­59.

Additional Growth Factor Research

Cosmetic and topical applications of growth factors

Photo damaged skin is the consequence of life long exposure to the sun. In fact, most changes in our aging skin are accelerated by the sun’s rays. These changes come in forms of wrinkles, dark spots, skin cancer, broken vessels, yellowing of skin tone, and leathery skin. Researches have noticed that photo damaged skin correlates with certain aspects of acute and chronic wound healing. Growth factors have demonstrated positive cosmetic and clinical outcomes of topical applications for photo damaged skin. Growth factors can initiate wound healing, promote new skin cell proliferation, increase collagen formation, stimulate formation of capillaries under the skin for oxygen delivery and participate in tissue rejuvenation on multiple levels of the skin. Growth factors may hold the key to reducing signs of skin aging and repairing photo damage.

Refer to references 60-­63.

Tendon, ligament, bone and connective tissue healing

Growth factors (bone morphogenetic protein, transforming growth factor 13, fibroblast growth factor, vascular endothelial, platelet derived growth factor, epidermal growth factor and insulin-like growth factor) can enhance fracture-healing rates in bones, ligaments, tendons and open wounds. Many growth factors in velvet antler initiate the tissue rebuilding process, while reducing inflammation and stimulating collagen production. Additionally, growth factors are present in multiple stages of the healing process and play a role in shortening and improving the recovery from tissue laceration, ruptures, tears and inflammation.

Refer to references 64-­68.

Nerve regenerating properties

Neurotropic factors isolated in velvet antler are polypeptides that support the growth,

differentiation and survival of neurons. These neuro-regenerative factors increase motor neuron activity and support catecholamine production that enhances neurotransmitters and nerve transmission. There is a belief that these growth factors could be used to treat mood disorders and even more severe complications of the peripheral nervous system like neurodegenerative diseases.

Refer to references 69-­71.