Nandrolone, Women and Cardiovascular Dysfunction

Nandrolone, Women, Cardiovascular Dysfunction. 

Life would be so much easier if we did not have to try to interpret ” indirect data” when it comes to AAS Harm Reduction Practices but that honestly is just wishful thinking…

This is simply our reality…

In this 2017 surrogate study they looked at the consequence on Cardiovascular Function when female Rats were administered Nandrolone ( ND )

The study showed new insights into the Cardiotoxic effects of ND.

The study showed that the chronic use of ND treatment induces endothelial dysfunction, which alters vascular responsiveness by a mechanism that involves NO pathway and possibly increased oxidative stress.

These findings add to the discussion that ND treatment might increase the risk for vascular injury in Women gender, a response that could predispose them to elevated risk of cardiovascular diseases

Now here IMO is the most important part of the study.

The study included the comparing the vascular reactivity profiles between female rats submitted to estrogen-deficiency animal models and Nandrolone exposure models

High doses of Nandrolone Decanoate induce vascular dysfunction in females very similar to the alterations observed in an estrogen deficiency model

” While we cannot discern whether the negative vascular effects observed in ND-treated females are due to a direct effect of ND or to an indirect effect of serum levels of testosterone and estrogen, the data does suggest that the reduction of circulating levels of estradiol in ND treated-females could lead to an impairment of vascular reactivity. “

My Takeway ?

Women have a better Cardiovascular Health Risk Profile than Men, and its Estrogen that provides that added Protection.

Submit female Rats to “Estrogen Deficiency” and they loose that Protection..

Submit female Rats to ” Nandrolone exposure” and they loose that Protection..

Estrogen is Cardiac Protective… in female Rats

In Women and in Men..

Nandrolone when used by itself – negates that Protection..

Long-term treatment with Nandrolone Decanoate impairs mesenteric vascular relaxation in both sedentary and exercised female rats


•  Nandrolone Decanoate (ND) impaired mesenteric vascular reactivity in female rats.
•  ND-induced vascular alterations were likely mediated by a reduction of NO pathway.
•  Exercise training did not improve the vascular alterations induced by ND treatment.
• ND led to vascular dysfunction similar to those found in ovariectomized female rats.Nandrolone Decanoate (ND) is an Anabolic Androgenic Steroid (AAS) that under abusive regimen can lead to multiple physiological adverse effects. Studies of AAS-mediated cardiovascular (CV) alterations were mostly taken from male subjects, even though women are also susceptible to the effects of AAS and gender-specific differences in susceptibility to vascular diseases exist. Here we investigate ND-induced vascular reactivity alterations in both sedentary and exercised female rats and whether these alterations depend on endothelium-derived factors. We show that chronic exposure of female Wistar rats to ND (20 mg/Kg/week for 4 weeks) impaired the vascular mesenteric bed (MVB) reactivity to vasodilator (acetylcholine) agonist. The endothelium-dependent Nitric Oxide (NO) component was reduced in ND-treated rats, whereas neither the endothelium-derived hyperpolarizing factor (EDHF) component nor prostanoids were altered in the MVBs. Endothelial dysfunction observed in ND-treated rats was associated with decreased eNOS (Ser1177) and Akt (Ser473) phosphorylation sites and upregulation of iNOS and NADPH oxidase expression. Exercise training by weight lifting in water did not improve the vascular alterations induced by ND treatment. ND treatment also significantly reduced the serum levels of estradiol in females, overriding its CV protective effect. These results help uncover the role of ND modulating endothelial function in the setting of CV disease caused by the abuse of AAS in females. If this translates to humans, young women abusing AAS can potentially lose the cardio protective effect rendered by estrogen and be more susceptible to CV alterations

Using Blood Pressure Medications in a Preventative Role for Left Ventricular Hypertrophy.

Using Blood Pressure Medications in a Preventative Role for Left Ventricular Hypertrophy.

This is a potentially very deep hole to open, but I have been meaning to broach the subject for some time… so lets open her up.

The effect of anabolic androgenic steroids on the cardiovascular system has been well described in the literature. The use of Anabolic Androgenic Steroids (AAS) has been linked to underlying a number of cardiac conditions

AAS like other endogenous steroids influence left ventricular hypertrophic response through the androgen receptor.

Androgen receptors are found on skeletal muscle and also on cardiac myocytes. They cause alterations in heart structure, including left ventricular hypertrophy, dilation which can cause impaired contraction and relaxation

Anabolic steroids can induce an unfavorable enlargement and thickening of the left ventricle, which loses its diastolic properties with the mass increase.

AAS can also cause hypertension, dyslipidemia, and impaired fasting glucose.

There is a case to be made for the use of ACE Inhibitors and ARBs in the preventing Left Ventricular Hypertrophy by
Hypertensive Patients

I am surprised that this is not a more common practice in AAS users.. in a preventative sense.

This conversation has the potential to spread into many ” separate discussions” from treatment of Steroid Induced LVH ( there case studies to look at ) to prevention.. to which ACE or ARB is best suited to the task and at what dosage.. along with the very practical ” what additional risks” if any would deployment present.

Anyone with initial comments.. most welcome.

Victor Black