The vast majority of Chronic Venous Insufficiency (CVI) sufferers are women (by approximately 10 to 1). Vein problems also tend to appear at an earlier age in women than in men. [Boccalon].
The prevalence and incidence of CVD vary among different populations. Varicose veins is predominantly a condition encountered in Western societies, and its incidence increases with age (Evans et al. 1994). Venous disorders of the lower extremity are rare in African or Australian aboriginal populations, where their incidence range from 0 to 5% (Stanhope 1975; Richardson & Dixon 1977). The results of several clinical and questionnaire studies suggest that varicosities are less common in non-Caucasian and underdeveloped countries than in Caucasian westernized societies, where the prevalence of lower-limb venous disease is high, as shown in Table 1 (Callam 1994). According to a recent article reviewing all papers on the epidemiological prevalence (1966-1999) of venous disease, increase with age is linear, suggesting a constant incidence and a cumulative prevalence (Adhikari et al. 2000).
Hormones are a factor, as well, causing weakness of the vein wall and valves. Hormonal changes occur during puberty, pregnancy, and menopause. Taking estrogen or progesterone supplement or birth control pills can cause women to develop vein disease.
Pregnancy not only boasts increased hormone levels, but there is also an increase in blood volume which can enlarge the veins. The enlarged uterus also puts pressure on the veins, therefore, the veins engorge with blood and dilate. This will weaken the vein and damage the vein valves.
Advancing age is also noted to be a factor in vein disease. Indeed, vein problems correlate significantly with increased age, with a significant number of people having vein disease by the time they are sixty years old.
Nutritional deficiencies of magnesium or zinc lead to a progressive and often marked growth retardation. We have evaluated the effect of Mg and Zn deficiency on growth, serum insulin-like growth factor-1 (s-IGF-1), growth hormone (s-GH) and insulin (s-insulin) in young rats. In 3-week-old rats maintained on Mg-deficient fodder for 12 d the weight gain was reduced by about 34%, compared with pair-fed controls. This was accompanied by a 44% reduction in s-IGF-1, while s-insulin showed no decrease. After 3 weeks on Mg-deficient fodder, growth had ceased while serum Mg (s-Mg) and s-IGF-1 were reduced by 76 and 60% respectively. Following repletion with Mg, s-Mg was completely normalized in 1 week, and s-IGF-1 reached control level after 2 weeks. Growth rate increased, but the rats had failed to catch up fully in weight after 3.5 weeks. Absolute and relative pair-feeding were compared during a Mg repletion experiment. Absolute pair-fed animals were given the same absolute amount of fodder as the Mg-deficient rats had consumed the day before. Relative pair-fed animals were given the same amount of fodder, on a body-weight basis, consumed in the Mg-deficient group the day before. In a repletion experiment the two methods did not differ significantly from each other with respect to body-weight, muscle weight, tibia length and s-IGF-1, although there was a tendency towards higher levels in the relative pair-fed group. The peak in s-GH after growth hormone-releasing factor 40 (GRF 40) was 336 (se 63) μg/l in 5-week-old rats that had been Mg depleted for 14 d, whereas age-matched control animals showed a peak of 363 (se 54) μg/l (not significant).
In 3-week-old rats maintained on Zn-deficient fodder for 14 d weight gain was reduced by 83% compared with pair-fed controls. Serum Zn (s-Zn) and s-IGF-1 were reduced by 80 and 69% respectively, while s-insulin was reduced by 66%. The Zn-deficient animals showed a more pronounced growth inhibition than that seen during Mg deficiency and after 17 d on Zn-deficient fodder s-IGF-1 was reduced by 83%. Following repletion with Zn, s-Zn was normalized and s-IGF-1 had increased by 194% (P <0.05) after 3 d. s-IGF-1, however, was not normalized until after 2.5 weeks of repletion. Growth rate increased but the catch-up in weight was not complete during 6 weeks. The maximum increase in s-GH after GRF 40 was 774 (se 61) μg/l in control animals ν. 657 (se 90) μg/l in 6-week-old rats that had been Zn-depleted for 12 d (not significant). In conclusion, both Mg and Zn deficiency lead to growth inhibition that is accompanied by reduced circulating s-IGF-1, but unchanged s-GH response. Zn deficiency, but not Mg deficiency, caused a reduction in s-insulin. The reduction in s-IGF-1 could not be attributed to reduced energy intake, but seems to be a specific effect of nutritional deficiency of Mg or Zn. It is suggested that the growth retardation seen during these deficiency states may be mediated through reduced s-IGF-1 production.
Taking estrogen or progesterone supplement or birth control pills can cause women to develop vein disease.
BACKGROUND: Sexual dysfunction in chronic renal failure patients undergoing hemodialysis is common. It is demonstrated that the zinc level is significantly lower in the hemodialysis patients.
OBJECTIVE: In this clinical trial, we investigate the effect of zinc supplement therapy on the serum levels of sexual hormones in hemodialysis male patients.
PATIENTS AND METHODS: We carried out a clinical trial study including 100 of our male patients with end-stage renal disease on hemodialysis. Testosterone, follicle-stimulating hormone (FSH), luteinizing hormone (LH), prolactin, and zinc plasma level were measured in all of the patients. The patients received zinc supplement (zinc sulfate, 250 mg/day) for 6 weeks, and sex hormones and zinc plasma level were checked again.
RESULTS: Serum level of FSH and prolactin did not have any significant changes before and after intervention, but serum level of testosterone, LH, and zinc increased significantly.
DISCUSSION: These results suggest that although zinc administration did not have a definite effect on hemodialysis patients with sexual dysfunction, it can cause increase in the serum level of sex hormones which may improve the sexual function of the patients in some aspects.
Zinc deficient humans and animals have depressed thymic mass and increased susceptibility to infection. In the present studies, we investigated the relationship between cellular immunity, thymic hormones, and serum zinc levels in 19 patients with common varied immunodeficiency. Five (26%) had serum zinc levels 2 SD below normal and 11 (58%) had abnormally low lymphocyte proliferation to at least one mitogen. A significant statistical correlation between zinc levels and lymphocyte proliferation to phytohemagglutinin and concanavalin A was identified. Forty-two percent had abnormally low levels of facteur thymique serique and 74% had low levels of thymopoietin, although no statistical relationship between the levels of these hormones, zinc levels, or lymphocyte proliferation could be identified. Three patients with the most profound zinc deficiency had substantial increases in thymic hormones after zinc repletion, and two had complete resolution of intractable diarrhea. A therapeutic potential of zinc for certain patients with hypogammaglobulinemia is suggested.
jimmylegs wrote:Taking estrogen or progesterone supplement or birth control pills can cause women to develop vein disease.
that would be, at very least in part, from the zinc depletion they cause, from the research i've seen.
Estrogen May Affect MS Risk
In the study, which appears in the Archives of Neurology, researchers looked at whether use of birth control pills or pregnancy in the last three years was associated with the risk of MS in a group of more than 106 women in Great Britain who were diagnosed with multiple sclerosis from 1993 to 2000.
Researchers compared the women with MS to more than 1,000 similar women without MS and found the risk of multiple sclerosis was 40% lower among women taking birth control pills compared with nonusers.
The study also showed that the risk of MS was slightly lower during pregnancy but nearly three times higher in the six months following pregnancy.
Researchers say the results suggest that high levels of estrogen -- such as during birth-control use and during pregnancy -- may delay or prevent multiple sclerosis.
The findings are also in line with previous studies in animals that have shown birth control pills, which contain estrogen, delayed the start of and eased the symptoms of MS.
Data from the Oxford. FPA prospective study show that oral contraceptive use and pregnancy have no discernible effect on the risk of developing multiple sclerosis (MS). Women of parity 0–2 developed MS twice as often as women of parity 3 or more but the difference did not reach statistical significance. Smoking may be a risk factor for developing MS. A nested case-control analysis did not identify any associations between MS onset and preceding illnesses.
For the second phase of analysis, all other relevant variables derived from the survey were reviewed to identify factors known or suspected to affect serum zinc concentration, independent of the zinc status of the subjects (ie, present or recent pregnancy or lactation; use of oral contraceptives, steroids, or other hormones; low serum albumin concentration; elevated or low white blood cell counts; diabetes; diarrhea; anemia; and cigarette smoking)... characteristics found to be associated with serum zinc concentration ... were as follows: low serum albumin (< 3.5 g/dL); high white blood cell count (> 11.5 × 109/L); current pregnancy or lactation (females aged 14–42 y only); current use of oral contraceptives (females aged ≥ 13 y)...
jimmylegs wrote:a ha! this will be interesting to unravel. re your wife, i'd be very interested to see results of a zinc test. or both copper and zinc. if it ever makes it onto your lady's agenda of course!
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