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Steroids and Health

Dirty Ancient Secrets
April 4, 2019
Lesbian Culture
March 15, 2019

How Taking Steroids Can Hurt Even Young, Healthy Guys

Growth Hormones

Your Heart Matters

For lots of guys, the promise of illegal anabolic steroids—that they'll help build muscle mass and strength—is just too strong. Worldwide, about 1 in 15 men have tried steroids at some point in their lives, a 2014 analysis of 271 studies concluded. And that number refers to men overall: The percentage for recreational athletes, including those who lift, is about three times higher.

While steroid use is pretty common, it’s not harmless. We've known for years that steroids can be dangerous, leading to issues like kidney failure, liver damage, and an enlarged heart, as well as shrinking testicles and lowered sperm counts.

Now, a new study adds further evidence that the illegal muscle builders may have serious consequences: Taking steroids could set the stage for a heart attack, new research presented at the Brazilian Congress of Cardiology suggests


In the study, researchers recruited 51 seemingly healthy men with an average age of 29 years old. Some lifted and took steroids, some lifted and didn’t take the drugs, and others were sedentary and did not take steroids. All took urine tests to make sure they reported their steroid use accurately, as well a CT scan to check out their arteries.

The results? About 1 in 4 lifters who took steroids had signs of atherosclerosis, or plaque buildup, in the arteries leading to their hearts. In comparison, none of the sedentary men or the lifters who did not use steroids showed buildup.

Plaque buildup is a big problem. If a piece of it breaks off and gets stuck in your bloodstream, it can block blood flow to your heart. And that can cause a heart attack, according to the American Heart Association.

The steroid users also had lower levels of HDL cholesterol, or the “good” kind, the researchers found. Having enough HDL cholesterol is important because it helps carry LDL, or the “bad” kind, out of your body before it can build up in your arteries.

It’s possible that anabolic steroids spark the activity of a certain enzyme in your liver that’s responsible for increasing LDL, or “bad” cholesterol, while tamping down the good kind, says study author Francis Ribeiro de Souza, Ph.D. (c), of the Heart Institute of the Medicine School of the University of São Paulo. The result is an imbalance of your good and bad cholesterol, which can lead to plaque formation.

Scary part is, some studies have suggested that the heart issues, like the hypertension and enlarged heart, may be irreversible, too, says Ribeiro de Souza (Here’s how to tell if someone is using steroids).

Larger studies are necessary to confirm the link between steroids and plaque buildup, but the results do seem to suggest that using the drugs can put even young, healthy men at risk for heart disease, he says.

The best—and incredibly obvious—way to protect your heart, then, is to avoid taking anabolic steroids (Want a safer way to build serious muscle? Try Metashred Extreme from Men’s Health—and make sure you’re not making these muscle-building mistakes).

If you’ve taken them in the past? Then it’s super important you come clean to your doctor about your history. He or she may recommend additional testing to monitor your heart for any possible problems, Ribeiro de Souza says.

Steroids were great… until my heart exploded at 34

REALITY star Spencer Matthews was booted out of the I’m A Celebrity jungle after confessing to a secret steroid addiction. Spencer admitted that he “screwed up” and took the pills for “vanity” and to bulk up before a celebrity boxing match.But the Made In Chelsea star, who has now gone into rehab, is not alone.

According to the Crime Survey for England and Wales, around 60,000 Brits take steroids, which mimic the effects of testosterone and boost muscle growth.But experts admit the true number of users could be far higher as many men keep their addiction under wraps.

ED 52 y.o

ED, a retired professional rugby player, from Folkestone, Kent, took steroids every day from the age of 16 to 34, when he suffered a heart attack. Ed, nicknamed “Spyk”, says:‘I was always a gifted athlete at school, winning at almost every sport I competed in. When I was 16, a friend introduced me to steroids.Instantly, I was hooked. I could exercise for longer, I packed on huge amounts of lean muscle and the girls came flocking.

I could see no downsides and when I started playing professional rugby in South Africa, I carried on using them religiously, either injecting or popping oral steroids every day. I didn’t become aggressive but I grew what are known as “b**** t*ts” because of the excess oestrogen in my body and these had to be surgically removed.I also had terrible acne on my back and my testicles shrunk to the size of peanuts.

But these things seemed a small price to pay for the attention, money and glamour I received for being so ripped. After retiring from rugby, I travelled to the US where I became a model and stuntman. I was loving life.

Everything changed one evening in 1997 when I was cooking dinner for my wife and my heart literally exploded – my aorta, the largest blood vessel in the body, had split in half from my heart all the way to my legs.

I faced the prospect of having both legs amputated and all the organs in my body were failing. I was in a coma for a month and in intensive care for two more. I had a series of operations to replace my aorta with a plastic one. In eight weeks, I went from 18st 1lb of solid muscle to 7st 7lb of skin and bone. I came round to find my wife had left me. My life had hit an all-time low.

After that I spent two years in bed recuperating, needing round-the-clock care. Then I spent five years in a wheelchair, slowly learning to walk again. I was told I would never be a father. Incredibly, I’m now off the steroids and I’ve managed to turn my life around.I have remarried and against all odds, I am now a dad to Angelyna, who is nine. In the past three years, I’ve had two more heart operations to keep me alive.

All I want to do now is share my story so other people don’t do what I did – nobody needs steroids. The day I had that first heart attack, when I was 34, I’d done over five hours of intensive training and I thought I was in the best shape of my life.

But nothing could have been further from the truth. I know tens of thousands of men out there are ticking bombs, waiting for their hearts to give in and leave their lives in ruins.I’ve lost three friends to steroids and seen countless more deal with the negative health issues,

family break-ups, job losses and more.Anyone who thinks steroids are an easy way to get big should think again because once you’re hooked psychologically and physically it’s unbelievably hard to stop. I tried to go cold turkey several times and couldn’t, despite knowing. My advice to Spencer, if he is taking steroids to get big, is to stop – and get professional help before it’s too late.’

Calvin Davidson, 28

CALVIN is a joiner from Montrose in Angus, Scotland, and lives with his partner Ainsley, who is 20 and a support for learning teacher. Calvin says: ‘I feel really sorry for Spencer Matthews – but frankly, to bulk up that quickly, you would have to be taking steroids.

I’ve seen pictures of him where he’s looked nothing like as muscular. Steroids have a dramatic effect on your muscle gain – but it comes at such a price. I’m lucky in that I never suffered “roid rage” – in my case, taking steroids just made me feel very depressed. I started muscle-building about a year and a half ago. Having been quite a chubby child, I was self- conscious about my weight and I wanted to finally get in shape.

But I couldn’t seem to build muscle quick enough, and I was constantly comparing myself to other guys at the gym. I was spending two hours a day lifting weights and doing cardio. I decided to start taking steroids so I could bulk up more quickly. I bought tablets called Anavar on the internet, and I took them for about four months. They cost more than £30 for a month’s supply but they had a dramatic effect on me.

I’m a level-headed guy, but I began to feel seriously depressed, and even more obsessed with working out at the gym. I was literally a danger to myself, and my family were very worried for me. I wasn’t in a relationship at the time, so that didn’t affect me, and thankfully I managed not to let it affect my work. But I realised that taking steroids was a dangerous game, and I stopped.I still work out just as hard, but I am trying to keep it in proportion.’

‘Dangerous addictive substances’

MEDICAL director of the Neca substance abuse health group DR ROB DAWSON says: “Spencer was lucky not to get arrested in Australia as possession of anabolic steroids is illegal there.

“These drugs are dangerous and addictive. Regular steroid abuse can lead to potentially dangerous conditions such as high blood pressure, blood clots or even heart attacks, particularly if used alongside cocaine, which is sadly common. “Infertility, acne, violent mood swings and hallucinations are all also possible results, with side-effects including liver damage, baldness, paranoia and gynomastia – the development of female breast tissue.

“Steroids are used for their muscle-building properties but are grossly overrated in what they purport to do and any gains are marginal. “There is a crisis of the male ego, in a sense. It’s about trying to re-assert masculinity.“We live in a disposable society where the idea of a fast-track to the body beautiful is appealing to some.“We are selling this idea to youngsters and the most vulnerable in society but we mustn’t inspire people to use them.”

The law

ANABOLIC steroids are Class C drugs, which are sold by pharmacists – but only to those with a valid doctor’s prescription. It is legal to possess or import steroids as long as they are for personal use.Possession with intent to supply – including giving the steroids to friends – is illegal and those found guilty could face up to 14 years in prison.

Corticosteroids, Heart Failure, and Hypertension: A Role for Immune Cells?

Aldosterone and its receptor the mineralocorticoid receptor (MR) are best known for their regulation of fluid and electrolyte homeostasis in epithelial cells. However, it is now clear that MR are also expressed in a broad range of nonepithelial tissues including the cardiovascular system.

In the heart and vascular tissues, pathological activation of MR promotes cardiovascular inflammation and remodeling for which there is increasing evidence that macrophages and other immune cells (e.g. T cells and dendritic cells) play a significant role. While the glucocorticoids and their receptors have well-described antiinflammatory actions in immune cells, a role for aldosterone and/or the MR in these cells is largely undefined.

Emerging evidence, however, suggests that MR signaling may directly or indirectly promote proinflammatory responses in these immune cells. This review will discuss the current understanding of the role of corticosteroid receptors in macrophages and their effect on cardiovascular diseases involving inflammation.

More people die from cardiovascular disease worldwide than any other cause with an estimated 17.3 million deaths per year . The prognosis of symptomatic heart failure remains dismal with average 1-yr and 5-yr mortality rates of 35% to 50%, respectively, despite major therapeutic advances. Moreover, the economic burden of heart failure is increasing globally in terms of healthcare requirements, disability, and premature deaths

Vascular and target organ inflammation from tissue injury has long been recognized to underlie the complex pathophysiology of cardiovascular disease regardless of the initiating event such as ischemia, autoimmunity, or activation of the renin-angiotensin-aldosterone system.

The immune system and endogenous corticosteroids are important modulators of this inflammatory process with recent studies describing a novel role for the macrophage mineralocorticoid receptor (MR) in modulating cardiac remodeling and systolic blood pressure

The aim of this review is to highlight the growing role of the immune system in modulating the outcome of MR signaling in cardiovascular tissues and of MR signaling in modulating the immune response.

Corticosteroids and Their Receptors

The corticosteroid receptors, glucocorticoid and mineralocorticoid receptors (GR and MR) are members of the steroid hormone receptor subgroup of the nuclear receptor superfamily of ligand-activated transcription factors .

A range of nongenomic responses have also been described for steroid hormone receptor and involve rapid intracellular signaling responses MR bind both endogenous glucocorticoids (cortisol in human, corticosterone in rodent) and mineralocorticoids (aldosterone) with high affinity


However, the epithelial MR selectivity for the physiological mineralocorticoids (e.g. aldosterone) is conferred by the enzyme 11β-hydroxysteroid dehydrogenase conversion of cortisol to cortisone, which is inactive at the MR (15, 16). In contrast, the absence of 11βHSD2 in nonepithelial tissues (e.g. cardiomyocytes, monocytes/macrophages) allows physiological glucocorticoids to modulate MR signaling in these tissues.

The specific role of MR signaling in these nonepithelial tissues is now recognized as an important mediator of cardiac pathology and a role for the nonepithelial MR as a second receptor for cortisol in normal physiology is increasingly being appreciated.

The corticosteroid hormones, via their effects on MR and GR, play an important role in cardiovascular inflammation. GR signaling is predominantly antiinflammatory in many systemic and local disease models, mainly due to its potent immunosuppressive effects.

Despite the postulated antiinflammatory benefits in cardiovascular tissues, adverse cardiovascular effects are seen in glucocorticoid excess states such as Cushing's syndrome and patients on therapeutic exogenous glucocorticoids. The effect of glucocorticoid excess on cardiovascular disease is complex and multifactorial, and the independent effects of GR signaling remain difficult to interrogate (reviewed in Ref. 17).

Whereas genomic and nongenomic MR regulation of proinflammatory and profibrotic pathways have been described in vascular endothelial and smooth muscle cells (18–20) and cardiomyocytes (21, 22), the exact role of the MR in immune cells such as macrophages has not been completely elucidated. Recent studies, however, suggest that MR signaling in macrophages also mediates proinflammatory and profibrotic gene expression This review will focus on MR-mediated cardiovascular pathology and the modulating role of the immune system on the underlying inflammation.

MR Activation and Cardiovascular Disease

Sustained activation of the MR by elevated aldosterone levels leads to cardiovascular dysfunction and pathology. Primary aldosteronism (PA) is characterized by autonomous mineralocorticoid excess and is a common cause of secondary hypertension (23, 24). Patients with primary aldosteronism experience disproportionately more cardiovascular events than those with essential hypertension matched for blood pressure levels

Under normal circumstances, MR signaling in renal tubules leads to sodium and water retention and thus maintains extracellular volume and blood pressure. Aldosterone excess mediates hypertension not only via potentiating renal effects but also via MR in the central nervous system (26, 27) and in the vascular


Activation of vascular MR directly regulates vascular tone and thus total peripheral resistance (28); in the longer term, elevated aldosterone contributes to remodeling of the vessel wall which, in turn, contributes to the maintenance of a higher blood pressure (19, 29, 30). Vascular smooth muscle cell (VSMC) MR can also independently regulate blood pressure in aged animals in which changes in renal sodium handling and vascular structure are unaffected (30).

The detrimental effects of MR activation in the heart are also clearly illustrated by clinical studies using MR antagonists. Large randomized controlled trials (RALES, EPHESUS, and EMPHASIS) have demonstrated the unequivocal mortality and morbidity benefits of MR antagonist treatment in both mild and moderately severe symptomatic heart failure, implicating MR signaling as a key mediator of heart disease.

However, the ligand responsible for MR activation had been the subject of debate given that circulating levels of aldosterone in these patients were barely elevated (35). This raises the possibility that the cardiovascular benefits conferred by aldosterone antagonists were at least partly independent of aldosterone itself and lend support to a role for cortisol in pathological states such as heart failure


Cardiac MR expression has also been found to be increased in failing hearts in humans and experimental animals . The clinical benefits of MR antagonists are further supported by extensive animal studies which illustrate the effects of an MR activated state on cardiac inflammation and remodeling after aldosterone or deoxycorticosterone (DOC) plus salt (aldosterone/salt, DOC/salt) or angiotensin II administration and/or l-nitro-arginine methyl ester (angiotensin II/l-NAME) .

These studies again show that mineralocorticoid-dependent and -independent MR activation promote tissue inflammation, remodeling, and left ventricular dysfunction. The current review aims to highlight the interactions between the immune system and cardiovascular tissue in both the clinical setting and these

experimental models.

MR Signaling in Cardiac Inflammation and Remodeling

Progressive heart failure is determined by pathological cardiac remodeling that occurs after tissue injury from myocardial infarct, acute or chronic inflammation, pressure and volume overload, and activation of the renin-angiotensin-aldosterone system (44).

MR activation promotes tissue oxidative stress and inflammation, which is characterized by a perivascular mononuclear infiltrate and increased adhesion markers with chemokine and cytokine expression This is a continuous process with subsequent remodeling and interstitial fibrosis.

Myocardial reduced nicotinamide adenine dinucleotide phosphate oxidase is a source of reactive oxygen species mediating oxidative stress that plays a significant role in cardiac pathology. Increased reduced nicotinamide adenine dinucleotide phosphate oxidase expression and activity are localized to cardiomyocytes and endothelium in heart failure (47, 48), and these are thought to activate redox-sensitive signaling pathways such as Src kinases and MAPK (ERK1/2) in pressure overload hypertrophy and failure (49)

. Inflammatory and fibrotic responses to aldosterone were blunted in Nox2-null mice, which were also shown to have reduced nuclear transcription factor-κB (NF-κB) activation (50). It has also been proposed that cardiomyocyte MR activation potentially leads to dysregulation of cellular handling of calcium, magnesium, and other ions, which induces high mitochondrial calcium and reactive oxygen species, resulting in necrosis and replacement fibrosis

Consistent with these studies, cardiomyocyte MR-null mice showed blunted oxidative stress and tissue injury responses to ischemia, suggesting that MR activation in these cells drives key oxidative responses (52, 53).

Activation and proliferation of fibroblasts in response to inflammatory cytokines and growth factors in high mineralocorticoid states promotes collagen deposition (fibrosis) leading to structural and functional remodeling in the myocardium (45, 46, 54). Repeated injury occurs with persistent inflammation and also leads to extensive interstitial scarring (55), which is reversible by MR antagonists

These models have also established that the remodeling benefits of MR blockade are independent of their blood pressure-lowering effects as well as plasma aldosterone level (57, 58). MR signaling in cardiomyocytes has also been shown to up-regulate genes involved in extracellular matrix remodeling

Recent studies with cardiomyocyte MR-null mice demonstrate protection from cardiac failure after pressure overload from transaortic constriction or coronary artery ligation (52, 61). Whereas the first study shows no protective effect on cardiac inflammation or fibrosis,

the latter demonstrates improvement in cardiac contractility, reduction in oxidative stress (see below), and protection from adverse remodeling with loss of cardiomyocyte MR. Similarly, cardiomyocyte MR-null mice are also protected from DOC/salt cardiac remodeling (53).

Together, these studies suggest that cardiomyocyte MR has a role in the regulation of structural and functional remodeling. In contrast, the lack of cardiac protection in fibroblast MR-null mice is consistent with the lack of functional MR in these cells (61).

Immune cells have now been shown to play a critical role in mediating proinflammatory and profibrotic effects in the setting of MR activation in cardiac tissues. MR are expressed in immune cells of the myeloid lineage including monocytes/macrophages (62), a subset of dendritic cells (63), and potentially neutrophils (64), making them nonclassical targets of aldosterone and potentially cortisol due to the absence of 11βHSD2

A significant inflammatory component with marked macrophage recruitment had been characterized in cardiovascular remodeling in MR-mediated and other cardiac pathophysiology (66–68). MR signaling induces oxidative stress in macrophages (69) via activation of NF-κB, which generates a proinflammatory macrophage phenotype (M1), responsible for amplifying tissue inflammation with consequent injury (39, 45)..

Although the dynamic nature of the macrophage phenotype in tissue injury and healing is not fully understood in the DOC/salt model, tissue repair and remodeling processes in other experimental disease models suggest M1 is subsequently replaced by profibrotic macrophage phenotype (M2) likely in response to tissue signals or T cell cytokines (70–72). .

M2 releases profibrotic factors involved in cardiac remodeling such as TGF-β, which promotes fibroblast activation and collagen deposition (73–75) (Fig. 1). We and others have demonstrated an independent and central role for MR in macrophages (7–9).

. Selective deletion of MR in these cells protects against adverse cardiac remodeling in the DOC/salt and angiotensin II or angiotensin II/L-NAME models of hypertension and, interestingly, also reduces infarct volume in the cerebral ischemia model (76). These highlight a central role for macrophage MR in the pathogenesis of tissue remodeling.

An important modulator of these macrophage functions is the T cell-macrophage interaction (71, 73, 74). However, the exact role of T cells in DOC/salt model of cardiac remodeling is uncertain. Potential mechanisms include direct regulation of dendritic cell MR by aldosterone to influence the differentiation of the CD4+ T helper cell (a subset of T cells) (63). CXCR4 antagonism was recently demonstrated to protect mice treated with DOC/salt from cardiac fibrosis and hypertension. .

Because CXCR4, a chemokine receptor, is widely expressed on T cells, this study suggests an important mechanistic role for T cells in MR-mediated disease (77). Studies from various disease models indicate that CD4+ T helper cells perform a key role in modulating the immune cell response in tissue inflammation and remodeling, e.g. T helper 1 (TH1) and T helper 2 cells (TH2) driving M1 and M2, respectively (78–81). .

Adoptive transfer of regulatory T helper cell (Treg) has also been shown to be cardiac protective in hypertensive mice treated with transaortic constriction by down-regulating immune response (82). The nature of the interaction between the various members of the immune system in MR-mediated pathology is an exciting and emerging area of research.

Immune Cells in MR-Mediated Cardiac Pathology: Insights from Transgenic Mice Models

Recently, Rickard et al. (7) and others (8, 9) demonstrated a role for macrophage MR and provided insights into macrophage phenotypes in cardiovascular remodeling by analyzing the effects of DOC/salt or angiotensin II/l-NAME treatment on transgenic mice with selective deletion in myeloid MR [myeloid MR knockout (MRKO)]. Given that cre recombinase is driven by the Lysozyme M promoter, this deletion affects cells of myeloid lineage, in particular monocytes, macrophages, and a subset of dendritic cells .

Peritoneal MR-null macrophages, elicited by thioglycolate stimulation, show reduced M1 but elevated M2 marker expression (9). Taken together with the demonstration of reduced inducible NOS-positive macrophages in hearts from l-NAME/salt-treated myeloid MRKO mice (8) as well as an earlier study by Keidar et al. (69), these data verify that MR signaling contributes to expression of proinflammatory M1 cytokines in macrophages.


Although there is a good suggestion that macrophages from myeloid MRKO adopt a typical M2 phenotype (9), other in vivo studies demonstrate a reduction in M1 markers but unchanged (rather than increased) M2 markers (7, 8), highlighting some variation in in vivo and ex vivo responses of the different macrophage populations..

These in vivo studies raise the possibility that macrophages from myeloid MRKO mice may be atypical M2 or M2-like (regulatory macrophages) phenotype because the mice were protected from cardiac fibrosis. In support, stimulation of myeloid MRKO macrophages with glucocorticoid, typically known to polarize macrophages toward M2-like phenotypes (73, 74), results in synergistic expression of M2 markers (9). .

This also illustrates the opposing effects of MR and GR signaling in macrophages. Therefore, more in vivo macrophage data are needed to verify the phenotype and function in the context of myeloid MRKO or general MR antagonism. It is likely that the chronic MR activation due to aldosterone or DOC in wild-type cardiac tissue yields a dynamic mixture of typical M1 and M2,.

and intermediate phenotypes at different phases of the remodeling process resulting in aberrant remodeling and fibrosis. Interrupting this process by generating atypical M2 or M2-like macrophages by MR KO intuitively accounts for the benefits seen in these studies .

The effect of myeloid MR deletion on dendritic cells in these models has not been explored. Studies using mice deficient in dendritic cells given DOC/salt model would enable assessment of the role of dendritic cells and may indirectly provide clues into the role of T cells in modulating immune responses to DOC/salt cardiovascular tissue remodeling.

MR-Mediated Inflammation and Remodeling in the Vessel Wall

Comprehensive reviews on MR signaling in the vessel wall have previously been published (29, 84). Vascular inflammation as a result of MR activation promotes recruitment of monocytes and lymphocytes via expression of vascular adhesion markers, chemokines, and cytokines (Fig. 2).

Activation of the vascular NF-κB and Rho-kinase signaling pathways by oxidative stress is thought to play an additional role. There is increasing evidence for a role for activated T cells in mediating vascular inflammation and hypertension in the setting of aldosterone treatment (85, 86).

Remodeling of the vessel wall contributes to the underlying pathophysiology of MR-mediated hypertension. Direct role of VSMC MR in blood pressure regulation has been demonstrated using mice with SMC-specific MR deficiency (30). MR signaling in VSMC stimulates migration, proliferation, and secretion of extracellular matrix (reviewed in Ref. 29).

Multiple factors such as angiotensin II, platelet derived growth factor, endothelin-1, and placental growth factor interact with MR and activate both genomic and nongenomic MR signaling pathways to result in remodeling (29, 87, 88). This leads to vascular fibrosis and stiffness that is characteristic of longstanding hypertension, particularly in patients with untreated and/or unrecognized PA.

Role of Macrophages in MR-Mediated Hypertension

Previous animal models have implicated macrophages as key players mediating vascular inflammation and hypertension. Mice studies employing techniques to exclude the presence of macrophages in tissues demonstrated reduced vascular inflammation, decreased oxidative stress and remodeling, and protection from hypertension when treated with angiotensin II (89, 90).

A role for macrophage MR signaling in blood pressure regulation has also been illustrated in studies involving macrophage MR deletion. These mice are clearly protected from DOC/salt-induced hypertension (7) but not in angiotensin II and/or l-NAME-dependent hypertension (8, 9)


These differences may reflect the direct vascular endothelial oxidative stress and inflammatory effects of l-NAME, independent of MR activation. Studies from this laboratory (7) suggest that macrophage MR play a pathogenic role in oxidative stress, inflammation, and vascular dysfunction, thus exacerbating hypertension.

Macrophages are a rich source of TGF-β, which is potentially up-regulated during MR-mediated vascular inflammation and injury. Recent in vivo studies demonstrate the ability of TGF-β to stimulate VSMC proliferation via downstream Smad3 signaling (91, 92). Thus, in addition to mediating vascular inflammation, macrophages may play a direct role in vascular remodeling and thus contribute to the persistence of hypertension.

Role of T cells in MR-Mediated Hypertension

There is mounting evidence for a role for T cells in hypertension. Guzik et al. (85) demonstrated that RAG-1 −/− mice (lacking T and B cells) are protected from both angiotensin II and DOC/salt-induced vascular inflammation and hypertension and that this can be reversed by adoptive transfer of T cells. However, a role for macrophages was not investigated


Madhur et al. (86) subsequently illustrated that infiltrating T cells in the vascular wall may be a TH17 subset by using IL-17−/− mice and showing loss of a pressor effect and preserved vascular function in response to angiotensin II. TH17 is a differentiated effector T helper cell, increasingly recognized for its role in many chronic inflammatory/autoimmune diseases (inflammatory bowel disease, rheumatoid arthritis, etc.) (93)


The provision of IL-6 and TGF-β by dendritic cells is critical for this TH17 differentiation (94). However, IL-17 production is enabled only after further priming by cytokines such as IL-23 or IL-1β (95, 96). Because macrophages are known to be a rich source of IL-23 or IL-1β, whether they interact with TH17 to promote the final functional phenotype in vascular tissues is currently uncertain.

A recent ex vivo study demonstrated bone marrow-derived dendritic cells treated with aldosterone are able to prime naive CD4+ T cells and promote TH17 differentiation (63). This highlights the functional significance of MR signaling in myeloid dendritic cells (97, 98) and the ability of aldosterone to indirectly promote TH17 differentiation. Vinh et al. (99)

demonstrated the critical role of costimulatory molecules (CD28/B7) in angiotensin II and DOC/salt-mediated hypertension, which points to the existence of T cell priming by dendritic cells. Thus one may propose the pathway of TH17 induction in Madhur's study (Fig. 2), which was not specifically designed to investigate the nature of the presented antigens or the specificity for TH17 priming.


The emerging role of immune cells in MR-mediated disease is one of the many areas that have expanded the role of MR beyond physiological salt and water regulation. Moreover, MR and GR signaling in macrophages and other nonepithelial tissues appear to have opposing effects. Thus the net effect of MR and GR signaling in macrophages (i.e. the immune response) may be determined,

in part, by the relative intracellular abundance of MR vs. GR ligands. Whereas the role of immune cells has been firmly established in other systemic disorders, and to a lesser extent in other cardiac disease models, our current understanding in MR-mediated cardiac models remains deficient. Nevertheless, the discovery of the role of immune cells in MR-mediated cardiac remodeling and hypertension

in several experimental mice models represents a new frontier in our research direction and understanding of its pathophysiology. Whether therapeutic selective immunomodulation, already in clinical practice for other autoimmune/inflammatory diseases, will be a useful novel approach in heart failure and hypertension remains to be seen.

Side Effects

Anabolic steroids are synthetic, or human-made, variations of the male sex hormone testosterone. The proper term for these compounds is anabolic-androgenic steroids. "Anabolic" refers to muscle building, and "androgenic" refers to increased male sex characteristics. Some common names for anabolic steroids are Gear, Juice, Roids, and Stackers.

Health care providers can prescribe steroids to treat hormonal issues, such as delayed puberty. Steroids can also treat diseases that cause muscle loss, such as cancer and AIDS. But some athletes and bodybuilders misuse these drugs in an attempt to boost performance or improve their physical appearance. The majority of people who misuse steroids are male weightlifters in their 20s or 30s. Anabolic steroid misuse is much less common in women. It is difficult to measure steroid misuse in the United States because many national surveys do not measure it. However, use among teens is generally minimal. The 2016 NIDA-funded Monitoring the Future study has shown that past-year misuse of steroids has declined among 8th and 10th graders in recent years, while holding steady for 12th graders.

How do people misuse anabolic steroids?

People who misuse anabolic steroids usually take them orally, inject them into muscles, or apply them to the skin as a gel or cream. These doses may be 10 to 100 times higher than doses prescribed to treat medical conditions.

cycling—taking multiple doses for a period of time, stopping for a time, and then restarting

stacking—combining two or more different steroids and mixing oral and/or injectable types

pyramiding—slowly increasing the dose or frequency of steroid misuse, reaching a peak amount, and then gradually tapering off to zero

plateauing—alternating, overlapping, or substituting with another steroid to avoid developing a toleranc

There is no scientific evidence that any of these practices reduce the harmful medical consequences of these drugs.

How do anabolic steroids affect the brain?

Anabolic steroids work differently from other drugs of abuse; they do not have the same short-term effects on the brain. The most important difference is that steroids do not directly activate the reward system to cause a “high”; they also do not trigger rapid increases in the brain chemical dopamine, which reinforces most other types of drug taking behavior. Misuse of anabolic steroids might lead to negative mental effects, such as:

paranoid (extreme, unreasonable) jealousy

extreme irritability and aggression (“roid rage”)

delusions—false beliefs or ideas

impaired judgment


What are other health effects of anabolic steroids?

Aside from mental effects, steroid use commonly causes severe acne. It also causes the body to swell, especially in the hands and feet.

Long-Term Effects Anabolic steroid misuse might lead to serious, even permanent, health problems such as:

kidney problems or failure

liver damage and tumors

enlarged heart, high blood pressure, and changes in blood cholesterol, all of which increase the risk of stroke and heart attack, even in young people increased risk of blood clots

shrinking testicles

decreased sperm count


development of breasts

increased risk for prostate cancer

Are anabolic steroids addictive?

Even though anabolic steroids do not cause the same high as other drugs, they can lead to a substance use disorder. A substance use disorder occurs when a person continues to misuse steroids, even though there are serious consequences for doing so. The most severe form of a substance use disorder is addiction.

People might continue to misuse steroids despite physical problems, high costs to buy the drugs, and negative effects on their relationships. These behaviors reflect steroids' addictive potential. Research has further found that some steroid users turn to other drugs, such as opioids, to reduce sleep problems and irritability caused by steroids.

How can people get treatment for anabolic steroid addiction?Some people seeking treatment for anabolic steroid addiction have found a combination of behavioral therapy and medications to be helpful.

In certain cases of addiction, patients have taken medicines to help treat symptoms of withdrawal. For example, health care providers have prescribed antidepressants to treat depression and pain medicines for headaches and muscle and joint pain. Other medicines have been used to help restore the patient's hormonal system.

Points to Remember

Anabolic steroids are synthetic variations of the male sex hormone testosterone


Health care providers can prescribe steroids to treat various medical conditions. But some athletes and bodybuilders misuse these drugs to boost performance or improve their physical appearance.

People who abuse anabolic steroids usually take them orally, inject them into the muscles, or apply them to the skin with a cream or gel.

People misuse steroids in a variety of doses and schedules.

Misuse of anabolic steroids might lead to short-term effects, including paranoid jealousy, extreme irritability and aggression, delusions, impaired judgement, and mania.

Continued steroid misuse can act on some of the same brain pathways and chemicals that are affected by other drugs, including dopamine, serotonin

, and opioid systems. Anabolic steroid misuse might lead to serious long-term, even permanent, health problems.

Several other effects are gender- and age-specific.

People who inject steroids increase their risk of contracting or transmitting HIV/AIDS or hepatitis


Even though anabolic steroids do not cause the same high as other drugs, they can lead to addiction.

Some people seeking treatment for anabolic steroid addiction have found behavioral therapy and medications to be helpful. Medicines can help treat

symptoms of withdrawal in some cases.

Growth hormone, athletic performance, and aging

Human growth hormone benefits, facts and fiction

Can human growth hormones really benefit aging, like the elusive fountain of youth? In 1513, the Spanish explorer Juan Ponce de Len arrived in Florida to search for the fountain of youth. If he got any benefit from his quest, it was due to the exercise involved in the search. Few men today believe in miraculous waters, but many, it seems, believe in the syringe of youth.

Instead of drinking rejuvenating waters, they inject human growth hormone to slow the tick of the clock. Some are motivated by the claims of the "anti-aging" movement, others by the examples of young athletes seeking a competitive edge. Like Ponce de Len, the athletes still get the benefit of exercise, while older men may use growth hormone shots as a substitute for working out. But will growth hormone boost performance or slow aging? And is it safe?

What is human growth hormone?

Growth hormone (GH) is a small protein that is made by the pituitary gland and secreted into the bloodstream. GH production is controlled by a complex set of hormones produced in the hypothalamus of the brain and in the intestinal tract and pancreas. The pituitary puts out GH in bursts; levels rise following exercise, trauma, and sleep.

Under normal conditions, more GH is produced at night than during the day. This physiology is complex, but at a minimum, it tells us that sporadic blood tests to measure GH levels are meaningless since high and low levels alternate throughout the day. But scientists who carefully measure overall GH production report that it rises during childhood, peaks during puberty, and declines from middle age onward


GH acts on many tissues throughout the body. In children and adolescents, it stimulates the growth of bone and cartilage. In people of all ages, GH boosts protein production, promotes the utilization of fat, interferes with the action of insulin, and raises blood sugar levels. GH also raises levels of insulin-like growth factor-1 (IGF-1).

Human growth hormone benefits

GH is available as a prescription drug that is administered by injection. GH is indicated for children with GH deficiency and others with very short stature. It is also approved to treat adult GH deficiency — an uncommon condition that almost always develops in conjunction with major problems afflicting the hypothalamus, pituitary gland, or both.

The diagnosis of adult GH deficiency depends on special tests that stimulate GH production; simple blood tests are useless at best, misleading at worst. Adults with bona fide GH deficiencies benefit from GH injections. They enjoy protection from fractures, increased muscle mass, improved exercise capacity and energy, and a reduced risk of future heart disease.

But there is a price to pay. Up to 30% of patients experience side effects that include fluid retention, joint and muscle pain, carpal tunnel syndrome (pressure on the nerve in the wrist causing hand pain and numbness), and high blood sugar levels.

HGH doping and athletic performance

Adults who are GH deficient get larger muscles, more energy, and improved exercise capacity from replacement therapy. Athletes work hard to build their muscles and enhance performance. Some also turn to GH. It's not an isolated problem. Despite being banned by the International Olympic Committee, Major League Baseball, the National Football League, and the World Anti-Doping Agency,

GH abuse has tainted many sports, including baseball, cycling, and track and field. Competitive athletes who abuse GH risk disqualification and disgrace. What do they gain in return? And do they also risk their health? Because GH use is banned and athletic performance depends on so many physical, psychological, and competitive factors, scientists have been unable to evaluate GH on the field. But they can conduct rando

A team of researchers from California conducted a detailed review of 44 high-quality studies of growth hormone in athletes. The subjects were young (average age 27), lean (average body mass index 24), and physically fit; 85% were male.

A total of 303 volunteers received GH injections, while 137 received placebo. After receiving daily injections for an average of 20 days, the subjects who received GH increased their lean body mass (which reflects muscle mass but can also include fluid mass) by an average of 4.6 pounds.

That's a big gain — but it did not translate into improved performance. In fact, GH did not produce measurable increases in either strength or exercise capacity. And the subjects who got GH were more likely to retain fluid and experience fatigue than were the volunteers who got the placebo.If you were a jock in high school or college,

you're likely to wince at the memory of your coach barking "no pain, no gain" to spur you on. Today, athletes who use illegal performance-enhancing drugs risk the pain of disqualification without proof of gain.

Human growth hormone and aging

To evaluate the safety and efficacy of GH in healthy older people, a team of researchers reviewed 31 high-quality studies that were completed after 1989. Each of the studies was small, but together they evaluated 220 subjects who received GH and 227 control subjects who did not get the hormone. Two-thirds of the subjects were men; their average age was 69, and the typical volunteer was overweight but not obese.

The dosage of GH varied considerably, and the duration of therapy ranged from two to 52 weeks. Still, the varying doses succeeded in boosting levels of IGF-1, which reflects the level of GH, by 88%. As compared to the subjects who did not get GH, the treated individuals gained an average of 4.6 pounds of lean body mass, and they shed a similar amount of body fat. There were no significant changes in LDL ("bad") cholesterol,

HDL ("good") cholesterol, triglycerides, aerobic capacity, bone density, or fasting blood sugar and insulin levels. But GH recipients experienced a high rate of side effects, including fluid retention, joint pain, breast enlargement, and carpal tunnel syndrome.

The studies were too short to detect any change in the risk of cancer, but other research suggests an increased risk of cancer in general and prostate cancer in particular.

To evaluate the safety and efficacy of GH in healthy older people, a team of researchers reviewed 31 high-quality studies that were completed after 1989. Each of the studies was small, but together they evaluated 220 subjects who received GH and 227 control subjects who did not get the hormone. Two-thirds of the subjects were men; their average age was 69, and the typical volunteer was overweight but not obese.

The dosage of GH varied considerably, and the duration of therapy ranged from two to 52 weeks. Still, the varying doses succeeded in boosting levels of IGF-1, which reflects the level of GH, by 88%. As compared to the subjects who did not get GH, the treated individuals gained an average of 4.6 pounds of lean body mass, and they shed a similar amount of body fat.

There were no significant changes in LDL ("bad") cholesterol, HDL ("good") cholesterol, triglycerides, aerobic capacity, bone density, or fasting blood sugar and insulin levels. But GH recipients experienced a high rate of side effects,

including fluid retention, joint pain, breast enlargement, and carpal tunnel syndrome. The studies were too short to detect any change in the risk of cancer, but other research suggests an increased risk of cancer in general and prostate cancer in particular.

HGH, or simple diet and exercise?

Aim for a moderate protein intake of about .36 grams per pound of body weight; even big men don't need more than 65 grams (about 2 ounces) a day, though athletes and men recovering from illnesses or surgery might do well with about 20% more.

Plan a balanced exercise regimen; aim for at least 30 minutes of moderate exercise, such as walking, a day, and be sure to add strength training two to three times a week to build muscle mass and strength. You'll reduce your risk of many chronic illnesses, enhance your vigor and enjoyment of life, and — it's true — slow the tick of the clock.>

Benefits of Human Growth Hormone, Including More Muscle & Less Fat

If you’re a sports fan, you’ve probably heard of human growth hormone — more commonly known as HGH — and associate it with cheating and steroid use. However, did you know that HGH is a natural testosterone booster that’s produced on its own and provides many important benefits? It’s true.

Human growth hormone is naturally produced in the pituitary gland and plays a vital role in cell regeneration, growth and maintaining healthy human tissue, including that of the brain and various vital organs. Once secreted, HGH remains active in the bloodstream for a few minutes, allowing just enough time for the liver to convert it into growth factors, the most crucial being insulin-like growth factor (IGF-1), which has growth-promoting properties on every cell in the body.

The study of human growth hormone is a little more than 100 years old, and synthetic human growth hormone was first developed in the 1980s and approved by the FDA for specific uses in adults and children. (1) Let’s find out why.

Increased Muscle Strength

Human growth hormone has been known to improve physical capacity of individuals through stimulating collagen synthesis in the skeletal muscle and tendons, increasing muscle strength and improving exercise performance as a result.

In the International Journal of Endocrinology, a study with 14 healthy men at the ages of 50 to 70 were randomized into two groups. Seven subjects were administered HGH therapy with seven placebo subjects, and they were re-evaluated after six months. After six months, there was a significant increase in the leg press responsiveness muscles in the growth hormone group.

Overall, the study concluded an increased muscle strength in the lower body after human growth hormone was administered in healthy men. In HGH-deficient adults, participants who were administered long-term HGH therapy experienced normalization of muscle strength, increased exercise capacity, and improved thermoregulation and body composition.

Better Fracture Healing

Numerous of local growth factors and hormones are responsible for regulating mineral and bone metabolism, along with fracture healing. Administration of human growth hormone has been shown to speed up the regeneration of bone, making it a key part of bone healing. Applying growth factors like IGF-1 is known to stimulate the metabolism of bone


In a study published in the journal BONE, growth hormone was systemically applied to recombinant species-specific rats by subcutaneous injections and was compared to the placebo group. As a result, the local growth factor application revealed a stronger effect on fracture healing than the systemic human growth hormone injection. These observations suggest that the local application of growth hormone speeds up fracture healing significantly without systemic adverse effects.

Human growth hormone plays a crucial role in the repair of wear and tear and expedites healing. Researchers have reported the beneficial effects of HGH in enhancing the healing of injuries and wounds significantly. A randomized, controlled, double-blinded study for six months of HGH therapy or placebo in 28 healthy older men with low baseline plasma IGF-1 was conducted at the University of California’s Department of Medicine.

As a result, healthy older men who were administered growth hormone had enhanced collagen deposition during the wound-healing process, helping the healing process.

Enhanced Weight Loss

Obese individuals have limited response to growth hormone stimuli release, and after successful reduction of weight, growth hormone responsiveness can be partial or complete. Growth hormone accelerates lipolysis, the breakdown of lipids and involves hydrolysis of triglycerides into glycerol and free fatty acids, and impaired secretion of human growth hormone leads to loss of lipolytic effect.

Dietary restrictions and growth hormone treatment effects on anabolic and lipolytic actions as well as the changes in growth hormone secretions and insulin were investigated in a study published in Hormone Research.

Twenty-four obese participants were on a hypocaloric diet and treated with recombinant human growth hormone or a placebo in a double-blinded, 12-week randomized study. As a result, growth hormone treatment caused a 1.6-fold increase in weight loss, with the greatest loss being visceral fat compared to the placebo.

In the placebo group, lean body mass was lost, whereas lean body mass was gained in the growth hormone group. This study suggests that in obese participants who eat a caloric-restriction diet, growth hormone accelerates the loss of body fat and improves growth hormone secretion. Thus, human growth hormone can serve a therapeutic role to help obese people lose weight.

Stronger Bones

The pituitary gland stimulates the release of growth hormone and is essential for regulating bone growth, especially during puberty. Growth hormone stimulates the production of IGF-1, which is produced in the liver and released in the blood.

With age, human growth hormone decreases and may be the cause of older individuals not being able to form or replace bone rapidly. The IGF-1/growth hormone duo stimulates bone-forming and bone-resorbing cells, leading to increased bone mass.

Reduced Cardiovascular Disease Risk

Adults who are growth hormone-deficient have an increased risk for cardiovascular disease, leading to decreased life expectancy. In Sweden, 104 patients who are growth hormone-deficient were studied for cardiovascular disease risk. These patients had higher body mass and triglyceride concentrations compared to controls. These results suggest lipoprotein metabolism is altered by growth hormone deficiency, increasing the risk for cardiovascular disease.

Improvement in Erectile Dysfunction

It’s been suggested in recent studies that human growth hormone is responsible for male reproductive function and sexual maturation while deficiency is associated with loss of sexual erection and desire.

Thirty-five healthy adult men and 45 participants with erectile dysfunction were exposed to tactile and visual stimuli in order to elicit penile tumescence in a German study. The increase in growth hormone was greater than 90 percent as determined during developing penile tumescence, followed by a transient decrease afterward.

This study suggests that penile erection may be induced by growth hormone through its stimulating activity on human corpus cavernosum smooth muscle, making it a potential natural remedy for impotence.

Decreased Obesity

Insulin resistance and visceral/abdominal obesity are common in adults with hormone growth deficiency. Abdominal obesity is prevalent in individuals who show low growth hormone and insulin-like growth hormone serum concentrations as well. Human growth hormone treatment has demonstrated positive results in adults who are growth hormone-deficient in treating obesity naturally.

Thirty men ages 48–66 with abdominal/visceral obesity were treated with recombinant human growth hormone in a nine-month, randomized, double-blind study published in the Journal of Clinical Endocrinology & Metabolism. Abdominal and visceral adipose tissue decreased along with diastolic blood pressure, and improved insulin sensitivity was one of the favorable benefits of human growth hormone found.

Better Mood and Cognitive FunctionBetter Mood and Cognitive Function

Quality of life and psychological well-being are restored when growth hormone therapy in growth hormone-deficient adults is administered. A Lithuanian study investigated the changes in cognitive function, mood and concentration from baseline after six months of treatment with human recombinant growth hormone. Eighteen adult patients with HGH deficiency participated in the study, and growth hormone was administered in 12 IU per week.

As a result, cognitive function and mood significantly increased after six months of therapy, according to mood scales. This study suggests that administering growth hormone can be a possible treatment option to improve cognitive function and mood in adults who are growth hormone-deficient.

Better Sleep

The majority of the growth hormone pulsatile secretion happens just after the onset of sleep and continues to rise when the first hours of sleep are reached. Individuals who are going through sleep deprivation, such as people who work the night shift or late studiers, can be affected negatively throughout the day. Lack of sleep alters pituitary and hypothalamus function, further altering growth hormone release time.

When sleep was deprived for 24 to 36 hours in a study conducted by the University of Chicago’s Department of Medicine, human growth hormone release was drastically decreased and noticeably decreased in growth hormone peak values at night

The 24-hour pulse rate of growth hormone became random and more frequent throughout these waking hours. This study suggests that sleep deprivation can reduce growth hormone release the morning after and can severely disturb and alter the sleep-wake cycle

Human Growth Hormone Deficiency

Signs and symptoms of growth hormone deficiency vary with age, and children can have different symptoms than an adult. Children being significantly shorter than children their age and grow less than two inches per year are common symptoms of growth hormone deficiency. Children with normal levels grow about 2.5 inches a year from age 1 until they hit puberty, when they can grow up to four inches a year.

However, a decline in human growth hormone does not have any impact on a child’s intelligence. Other symptoms of growth hormone deficiency in children include:

Facial features may appear younger than children who are the same age

Delayed puberty, sometimes will not go through puberty

Increased fat around the stomach and face

Prominent forehead

Slow hair growth

Adults may experience a combination of symptoms from human growth hormone deficiency, including:


Hair loss

Sexual dysfunction

Decreased muscle strength and mass

Memory loss

Lack of concentration

Dry skin

Increased triglycerides


Cardiovascular disease risk

Reduced bone density

Temperature sensitivities

Increased weight, especially around the waist

Impact of Human Growth Hormone of Men and Women

More women are now using HGH for its anti-aging and weight-loss properties. Deficiency in human growth hormone in women is due to pituitary gland not producing enough HGH.

In women, human growth hormone levels start to decline in their early 20s, and signs of HGH deficiency include dry skin, thinning hair, greater belly fat and the development of wrinkles.

It’s been reported in studies that women secrete greater amounts of growth hormone than men, despite having similar reference ranges of serum IGF-1. Recently, there are significant clinical differences in the responses of HGH treatment in adults with HGH deficiency and a need to adjust the dose of recombinant human growth hormone.

Adequate HGH levels help women improve an appropriate body-fat ratio and elasticity in skin. Risk of osteoporosis is reduced when HGH levels in women are balanced. Intramuscular HGH injections can help normalize sleep patterns, improved skin elasticity, help lose excess fat and enhance the immune system.

Men are likely to feel the first signs of aging after 35 old, such as loss of libido, weakness, baldness and memory loss. Human growth hormone has a positive impact on men, giving them the physical ability to perform in sports, which is why men often go through HGH treatment during intense training.

Men who are treated with HGH experience reduction of fat, skin tightening, hair becomes healthier and thicker, and erectile dysfunction is corrected.

Best Ways to Increase HGH Naturally

High-Intensity Exercise

It’s well-documented in variou studies that exercise-induced growth hormone response increases HGH secretion. Research suggests that the exercise-induced growth hormone plus endurance exercise associated with load, intensity, duration and frequency are the determining factors in the regulation of HGH secretion.

An exercise intensity above lactate threshold and for a minimum of 10 minutes elicits the greatest stimulus to the secretion of HGH. HIIT workouts are effective in promoting beneficial well-being, health and positive training outcomes, while stimulating HGH.


Supplementing with L-glutamine is known for enhancing exercise performance, maintaining acid-base balance and increasing the storage of glycogen in muscle. In an Iranian study, 30 healthy non-athlete males were randomly divided into placebo and glutamine supplementation groups and put through an eight-week resistance training program.

Both groups performed the same weight training program three days a week for eight weeks. Both groups increased in performance, but the glutamine groups showed greater increases in lower- and upper-body strength, explosive muscle power, blood testosterone, IGF-1, and HGH compared to the placebo group.


Most studies have shown when administering oral L-arginine to participants, arginine alone increases the resting growth hormone levels at least 100 percent, while exercise can increase growth hormone levels by 300 percent to 500 percent.


According to a study in the 2008 issue of the Journal of the International Society of Sports Nutrition, alpha-glycerylphosphorylcholine (A-GPC) might increase human growth hormone levels. Participants who consumed 600 milligrams of A-GPC two hours before resistance exercise had increased HGH levels post-exercise compared to those given a placebo


Researchers Stanley Tan and Lee Berk at Loma Linda University in Loma Linda, Calif., observed that two hormones, human growth hormone and endorphins, were increased by 27 percent and 87 percent, respectively, when participants anticipated watching a humorous video.

Liver Detox

HGH stimulates the liver into producing IGF-1, which is released into the body to stimulate the production of cells that are responsible for cell proliferation, increased muscle mass and increased energy.

An individual would never experience the full benefits HGH has to offer if experiencing poor liver function, cirrhosis, fatty liver and non-alcoholic fatty liver disease. (20) Thus, if you naturally want to increase HGH, you should go on a liver

Vitamin C

Studies have observed the correlation of reduced vitamin C concentration in decreased growth hormone secretion, obese patients, increased waist-hip ratio and increased heart disease risk, which is why consuming more vitamin C foods may help increase HGH

Human Growth Hormone Precautions

Unfortunately, HGH has side effects. Major side effects include enlargement of the fingers and toes, skeletal changes, growth of the orbit, and lengthening of the jaw. The internal organs also can enlarge, and cardiomegaly is often one of the causes of death associated with HGH abuse.

Since skeletal muscle increases in size, there are often complaints of muscle weakness and occasional feeling of “pins and needles” sensation, known as carpal tunnel syndrome, which are particularly observed by individuals who take daily doses of four IU of HGH or higher.

Individuals also notice fingers feeling swollen or face feeling fuller at doses of four IU and above. This side effect is temporary and has been shown to go away when the dose is lowered within two weeks after the cycle is discontinued.

Another consequence of increased protein synthesis during HGH abuse includes changes to the skin, such as thickening and coarsening, known as “elephant epidermis.” The combination of side effects, particularly cardiomegaly, hyperlipidemia, hyperglycemia, usually contributes to a shortened life span in those suffering from overproduction of HGH

Final Thoughts on Human Growth Hormone

The use of human growth hormone and the research confirming its anti-aging and performance-enhancing properties has increased throughout the years.

Symptoms of human growth hormone deficiency include depression, fatigue, decreased muscle strength and mass, insulin resistance, hair loss, cardiovascular disease risk, memory loss, and delayed puberty in children.

Increased energy levels, exercise performance, lean muscle mass, hair growth and stronger bones are few of the many benefits of human growth hormone.

Natural ways to boost human growth hormone levels include laughter, sleep, liver detox, L-arginine, L-glutamine and exercise.

M I Ro

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