Pro-Cell 40 Research

Currently, the research in this document has been taken straight from a DEDI Pro-Cell 40 report book. This report was intended for health care professionals, scientists, and doctors. The content has not been altered and contains complex scientific terminology not meant to describe Pro-Cell 40 to the public. Strictly Supplements will convert the text to terms easily understandable to all who wish to learn about Pro-Cell 40 in the near future. Also note this page only contains a section of DEDI's report.

The following indications have been investigated regarding this product:

Influence of DHEA on the growth of MCD-7 human breast cancer cells in vitro
Opposing actions of DHEA and testosterone on insulin sensitivity in vivo and in vitro
Postmenopausal steroid replacement with micronized DHEA
Relationship of serum DHEA and postmenopausal breast cancer
Pituitary secretory activity following DHEA administration
DHEA administration stimulates cervical ripening
Protection against acute lethal viral infection with DHEA
DHEA as an inhibitor of Epstein-Barr virus-induced transformation of human lymphocytes
Effect of DHEA in lymphocytes and macrophages infected with HIV

Summary and Analysis of Data from Published Reports

Loria RM, Inge TH, Cook SS, Szakal AK, Regelson W: Protection against acute Lethal Viral Infections with the Native Steroid Dehydroepiandrosterone (DHEA); Journal of Medical Virology 26:301-314 (1988) (Abstract)

"A significant protective effect of native adrenal steroid, dehydroepiandrosterone (DHEA), was demonstrated in studies of two lethal viral infection models in mice: systemic coxsackievirus B4 and herpes simplex type 2 encephalitis. The steroid was active either by long-term feeding or by a single subcutaneous injection. A closely related steroid, etiocholanolone, was not protective in these models. Histopathological analysis, leukocyte counts, and numbers of spleen antibody forming cells in the coxsackievirus B4 model suggest that DHEA functions by maintaining or potentiating the immune competence of mice otherwise depressed by viral infection. DHEA was not effective in genetically immunodeficient HRS/J hr/hr mice and did not demonstrate antiviral activity in vitro. While the molecular basis for DHEA's effect on the immune system is not known, studies by others suggest that it may counteract the stress related immunosuppressive effects of glucocorticoids stimulated by viral infection. Because DHEA is a native steroid that has been used clincially with minimal side effects, the utility of DHEA in he therapeutic modulation of acute and chronic viral infections including the acquired immune deficiency syndrome deserves intensive study."

Henderson E, Schwartz A, Pashko L, Abou-Gharbia M, Swern D: Dehydroepiandrosterone and 16a-bromo-epiandrosterone: inhibitors of Epstein-Barr virus-induced transformation of human lymphocytes; Carcinogenesis, Vol 2(7)683-6 (1981) (Abstract)

"Dehydroepiandrosterone (DHEA), a major adrenal secretory product in men and women, is a potent inhibitor of mammalian glucose-6-phosphate dehydrogenase (G6PHD). Long-term treatment with this steroid has previously been found to suppress spontaneous breast cancer development in C3H mice. DHEA is now shown to inhibit Epstein-Barr virus (EBV)-induced morphologic transformation and stimulation of DNA synthesis in human lymphocytes. 16aBr-epiandrosterone, a DHEA analog that is about 60 times as potent as DHEA as an inhibitor of G6PDH, is much more effective as an inhibitor of EBV-induced transformation."

Membreno L, Irony I, Dere W, Klein R, Biglieri EG, Cobb E: Adrenocortical Function in Acquired Immunodeficiency Syndrome; Journal of Clinical Endrocrinology and Metabolism 65(3)482-7 (1987) (Abstract)

"Clinical features of adrenal steroid deficiency occur in patients with the acquired immunodeficiency syndrome (AIDS). To determine the frequency of aberrations in peripheral steroid levels in patients with AIDS and AIDS-related complex (ARC) we measured morning recumbent plasma cortisol, deoxycorticosterone, aldosterone, and 18-hydroxycorticosterone concentrations before and after administration of 0.25 mg ACTH (Cosyntropin) in 74 randomly selected hospitalized patients with AIDS and 19 patients with ARD. Basal (0800 h) cortisol levels in the AIDS patients were significantly higher (P 0.01) than those in normal subjects, while other ACTHdependent steroids of the 17-deoxypathway, deoxycorticosterone, corticosteron, and 18-OHDOC, were normal. These latter steroids increased subnormally in response to ACTH in patients with either AIDS (P<0.001) or ARC (P<0.005), but in ARc patients plasma 18-OHDOC levels were significantly higher than in those with AIDS (P&0.001). Supraphysiological doses of ACTH were then administered for 3 consecutive days to 14 patients with AIDS and 9 with ARC, which confirmed and amplified he subnormal responses of these steroids in AIDS. The mean plasma cortisol response was reduced on the third day only in AIDS Patients, whereas in the ARC patients the steroid responses were normal. Angiotensin III infusion and postural stimulation increased plasma aldosterone and 18-hydroxycorticosterone levels in AIDS and ARC patients. Defective stimulation of 18-OHDOC alone or in combination with defective stimulation of other 17-deoxysteroids can be a harbinger of subsequent impaired adrenal capacity in AIDS."

Polk BF, Fox R, et al: Predictors of the acquired immunodeficiency syndrome developing in a cohort of seropositive homosexual men; The New England Journal oF Medicine 316(2)61-6 (1987) (Abstract)

"In a cohort of 1935 homosexual men who were seropositive for human immunodeficiency virus (HIV) on entry into a prospective study, the acquired immunodeficiency syndrome (AIDS) developed in 59 during a median follow-up of 15 months. We matched 5 seropositive controls to each case according to study center and date of enrollment and performed a case-control analysis to determine factors predictive of AIDS.

In a multivariate analysis, a decreased number of T helper lymphocytes, an increased number T suppressor lymphocytes, a low level of antibody to HIV, a high titer of cytomegalovirus antibody, and a history of sex with someone in whom AIDS developed were independently associated with subsequent AIDS. Separate analyses of risk factors for Kaposi's sarcoma and opportunistic infections failed to support previously reported associates between the use of nitrites or an elevated cytomegalovius-antibody titer and Kaposi's sarcoma. These variables may be markers rather than determinants of disease progression. A vigorous antibody response to HIV infection may confer at least temporary protection against the progression of immunodeficiency to AIDS, or a low level of antibody to HIV may reflect a later stage of infection. The increased risk associated with a history of sex with someone in whom AIDS developed may indicate earlier infection in cases or infection with a more virulent strain of HIV. These results may be useful in counseling HIV-seropositive persons and in designing studies of clinical interventions."

Moss AR, Bacchetti P, Osmond D, et al: Seropositivity for HIV and the development of AIDS or AIDS related condition: three year follow up of the San Francisco General Hospital cohort; British Medical Journal 296, 745-750 (1988) (Abstract)

"The three year actuarial progression rate to the acquired immune deficiency syndrome (AIDS) in a cohort of men in San Francisco who were seropositive for the human immuno-deficiency virus (HIV) was 22%. An additional 26 (19%) developed AIDS related conditions. Beta₂-Microglobulin concentration, packed cell volume, HIV _p24 antigenaemia, and the proportion and number of T4 lymphocytes each independently predicted progression to AIDS. Beta₂-Microclobulin was the most powerful predictor. The 111 subjects tested who were normal by all predictors (40% had a three years progression rate of 7%, and the 68 subjects who were abnormal by two or more predictors (24%) had a progression rate of 57%. Two thirds of all men who progressed to AIDS were in the last group. The median T4 lymphocyte count in subjects who did not progress to AIDS fell from 626x10⁶ to 327x10⁶/1. HiV _p24 antigenaemia developed in 7% of the subjects per year. The proportion who where abnormal by two or more predictive variables rose to 41%. At three years an estimated two thirds of the seropositive subjects showed clinical AIDS, and AIDS related condition, or laboratory results that were highly predictive of AIDS.

It is concluded from the observed rates and the distribution of predictive variables at three years that half of the men who were seropositive for HIV will develop AIDS by six years after the start of the study, and three quarters will develop AIDS or an AIDS related condition."

This page is under construction. The majority of DEDI's report that remains will be added shortly and deciphered soon after.