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Biomedical subjects

B A Stoll

Publications and source records attributed to B A Stoll.

At least 37 records · Page 2Linked to original sources
PubMed1997

Eating to beat breast cancer: potential role for soy supplements.

BACKGROUND: The study reviews the anticancer properties of natural isoflavones which occur in especially high concentration in soybeans. It considers the suitability of soybean products for clinical trials aiming to reduce the progression of breast cancer. METHODS: Evidence is reviewed that plant isoflavones such as genistein show cytostatic activity against human mammary cancer cell lines in vitro and can also suppress carcinogen-induced mammary cancer in young and mature rats. RESULTS: Plant isoflavones are converted in the bowel to compounds with potential antioestrogenic and antioxidative properties. These compounds show cytostatic activity for both oestrogen receptor-positive and negative human mammary cancer cell lines, and also inhibit growth and progress of the rat mammary cancer model. The high content of soybean products in the diet of Asian women has been postulated as one reason for their relatively low breast cancer incidence. CONCLUSION: Preclinical studies suggest that soybean products be given priority for clinical trials in breast cancer protection. A pilot study could test soy protein supplements as long-term adjuvant dietary treatment after primary surgery for early breast cancer, looking for a decrease in the risk of recurrence or of second primary tumours.

Anticarcinogenic Agents↗
PubMed1997

Breast cancer: further metabolic-endocrine risk markers?

There is evidence that increased oestrogen receptor (ER) expression in normal mammary epithelium may be a risk marker for the development of breast cancer. Insulin-like growth factor 1 (IGF1) is a potent inducer of mitosis and has been shown to synergize with oestrogen in stimulating the growth of human breast cancer in vitro. In these cells oestradiol has been shown to upregulate IGF type 1 receptor (IGFR), and recently a similar effect has been reported in normal human breast tissue xenografts in vivo. It has been postulated that the combined effect of oestradiol and IGF1 may stimulate proliferation in normal mammary epithelium and increase breast cancer risk. The bioavailability of IGF1 to the tissues is modulated by IGF-binding proteins (IGFBPs), and higher circulating levels of IGF1 and lower levels of IGFBP3 have been reported in breast cancer patients. Breast cancer specimens show a positive correlation between ER status and IGF receptor status, and also a negative correlation between ER status and IGFBP3 expression. Finally, ectopic growth hormone expression has been shown in a majority of specimens of normal and malignant breast tissue, and this may contribute to breast cancer risk, possibly by increasing the local level of bioavailable IGF1. Expansion of such findings may provide clinically useful markers of increased risk to breast cancer in women.

Breast Neoplasms↗
PubMed1997

Macronutrient supplements may reduce breast cancer risk: how, when and which?

OBJECTIVE: To examine evidence that specific fibre-associated macronutrients are associated with a decreased breast cancer risk. To review possible mechanisms, the age group when dietary intervention might be most effective and the choice of a suitable dietary supplement. DESIGN: This review distinguishes specific hormone-metabolic effects of dietary composition from those of body mass and fat distribution, in relation to the age at which they exert major effects on breast cancer risk. RESULTS: Both obesity and a high-fat/low-fibre diet in Western women may be associated with increased estrogen levels which are widely assumed to increase the risk of developing breast cancer. Both obesity and the Western diet are likely to stimulate insulin resistance, leading to increased levels of bioavailable estrogen. The concomitants of hyperinsulinemia may synergize with estrogen in stimulating progression of pre-neoplastic lesions in the breasts of late pre-menopausal women. Increased intake of fibre-associated macronutrients may reduce insulin resistance in addition to reducing the circulating levels of estrogen. CONCLUSIONS: The effect of dietary intervention on breast cancer risk in Western women may be tested in pre-menopausal women over the age of 40 y, with evidence of atypical hyperplasia in a breast biopsy. The most suitable fibre-associated macronutrient is still problematical but soy protein constituents have been shown to inhibit the growth of rat mammary cancer models and also of human breast cancer cell line in the laboratory.

Adolescent↗
PubMed1996

Diet and exercise regimens to improve breast carcinoma prognosis.

BACKGROUND: Clinical studies agree that obesity worsens the prognosis of breast carcinoma in both pre- and postmenopausal women. There is considerable evidence that free estrogen levels are raised in obese women, especially in those with abdominal (visceral) obesity and hyperinsulinemic insulin resistance. It has been postulated that estrogen may synergize with the concomitants of hyperinsulinemia in stimulating breast carcinoma growth. Reduction of estrogen and insulin levels may slow this growth. METHODS: A current clinical trial in the U.S. is examining the effect of dietary fat reduction on recurrence and survival rates after primary treatment of early stage breast carcinoma in postmenopausal women. Recent research suggests that a high fiber/fat ratio in the diet and regular physical exercise may help to reduce estrogen and insulin levels. Regular exercise may also help to maintain long term weight loss. RESULTS: A second-generation trial is proposed of a high fiber, low fat diet associated with regular physical exercise in women with early breast carcinoma. Changes in circulating levels of estrogen and insulin will be monitored in relation to timing of tumor recurrence and second primary breast carcinoma rates. Weight and fat distribution will be monitored in relation to measurements of dietary compliance. CONCLUSIONS: Breast carcinoma patients wishing to change their lifestyle are likely to benefit from a higher dietary fiber/fat ratio combined with regular physical exercise. If the trial shows an improved prognosis from intervention correlated with changes in biomarkers, a similar trial model could be used to identify specific fiber supplements, micronutrients, and exercise regimens that may improve survival rates in patients with breast carcinoma.

Breast Neoplasms↗
PubMed1996

Nutrition and breast cancer risk: can an effect via insulin resistance be demonstrated?

It is postulated that the metabolic/endocrine concomitants of insulin resistance resulting from high animal fat intake and weight gain after the age of 30 could be contributing to the increasing incidence of postmenopausal breast cancer and recent changes in its biologic characteristics. Case/control studies have shown that hyperinsulinaemia and abdominal obesity, which are recognized as markers of insulin resistance, are risk markers for postmenopausal breast cancer also. Excess weight gain linked to high dietary intake of saturated fat is thought to be a major cause of insulin resistance. The hypothesis is compatible with the "breast tissue age" model for breast cancer risk. Biological evidence suggests that the concomitants of insulin resistance may stimulate growth activity in existing breast cancer also. The hypothesis that nutritional factors which favour hyperinsulinaemia may also favour breast cancer growth can be tested. Restriction of dietary fat and high intake of fibre and complex carbohydrate have been shown to normalise insulin levels in a proportion of subjects with hyperinsulinaemia. Restriction of dietary fat intake has also been shown to reduce bioavailable oestrogen levels in healthy postmenopausal women. A randomised trial of a low fat, high fibre, high complex carbohydrate regimen is proposed as adjuvant treatment following primary surgery in postmenopausal women with early breast cancer. A cancer preventive or delaying ability can be assessed by comparing the incidence of contralateral second breast cancer and the metastasis rate in the diet and control groups. Insulin levels, abdominal obesity, and body mass should be monitored although normalisation of insulin levels need not necessarily involve decrease in body mass.

Breast Neoplasms↗
PubMed1996

Can supplementary dietary fibre suppress breast cancer growth?

Case-control studies in diverse populations around the world have reported a lower risk of breast cancer in association with higher intake of dietary fibre and complex carbohydrates. Although this has not been confirmed in prospective studies in the USA, the observations have prompted the hypothesis that prolonged use of dietary fibre supplements might reduce breast cancer risk in high-incidence populations. Several possible mechanisms of action have been suggested, all involving a reduction of bioactive oestrogen levels in the blood. The various mechanisms are not necessarily mutually exclusive. First, a high-fibre diet might reduce circulating oestrogen levels by reducing the enterohepatic recirculation of oestrogen. Second, many plants and vegetables contain isoflavones and lignans capable of conversion in the bowel into weak oestrogens that may compete with oestradiol for target binding-sites. Third, a high-fibre diet is less often associated with obesity, which tends to increase availability of the biologically active 16-alpha metabolites of oestrone. Fourth, a high-fibre diet usually has a lower content of fat and a higher content of antioxidant vitamins, which may protect against breast cancer risk. Finally, diets rich in fibre and complex carbohydrates have been shown to improve insulin sensitivity, with an associated reduction in circulating oestrogen levels. Synergism between these effects offers a possible mechanism by which a high fibre intake might suppress breast cancer growth in women.

Breast Neoplasms↗
PubMed1996

Obesity and breast cancer.

The high incidence of breast cancer in Western women has been linked to nutritional factors such as high-fat/low-fibre diet, obesity and timing of weight gain. A mechanism is postulated through which the Western diet could act in conjunction with inadequate exercise and excessive weight gain at the time of a major change in hormonal balance. All these factors favour the manifestation of insulin resistance, and the concomitants of hyperinsulinaemia might then synergise with oestrogen in promoting the development of breast cancer. The mechanism is compatible with the 'breast tissue age' model of mammary carcinogenesis. The concomitants of hyperinsulinaemia could also influence the growth of established disease subsequent to its promotion, and it is suggested that the hypothesis be tested by an adjuvant randomised trial of a high-fibre/low-fat diet in patients following primary surgery for early breast cancer. It has been suggested that the development of insulin resistance may link the Western lifestyle not only to an increased risk of hypertension and arteriosclerosis, but also to increased breast cancer risk. Large abdominal fat deposits in women are frequently a marker of the presence of insulin resistance and are generally associated with an increased level of bio-available oestrogen. There is evidence that predominantly abdominal distribution of fat in women may be a marker of increased breast cancer risk from puberty onwards. Abdominal obesity may however be hidden, and it is more reliably demonstrated by imaging techniques such as CAT or MRI scans, than by anthropometric measurements such as increased waist-to-hip ratio.

Breast Neoplasms↗
PubMed1995

Timing of weight gain in relation to breast cancer risk.

Excessive weight gain in women at the time of intense hormonal change can result in metabolic dysfunction. The metabolic/endocrine effect of puberty, pregnancy or menopause on breast tissue 'aging' is likely to be more relevant to a woman's breast cancer risk than is her degree of obesity at the time when the cancer presents. Experimental evidence suggests that the susceptibility of mammary tissue to carcinogenesis is greatest in early adult life, and multiple studies show that a history of weight gain in early adult life is associated with increased breast cancer risk in Western women. Excessive weight gain in that age group is associated with the development of hyperinsulinaemia in individuals with genetic susceptibility to insulin resistance. The insulin resistance syndrome may be a metabolic link between weight gain and breast cancer risk in Western women. Some studies suggest that in postmenopausal women, hyperinsulinaemia is related more to overall obesity, whereas in premenopausal women it is related more to abdominal localisation of fat. This may explain why an increased body mass index is a risk marker for breast cancer in postmenopausal but not premenopausal women. (A premenopausal woman with an average body mass index may have a large intra-abdominal fat mass associated with the presence of hyperinsulinaemia.) It is hypothesised that over-nutrition and inadequate physical exercise favour the development of hyperinsulinaemia and also increase breast cancer risk in women with a genetic susceptibility to both conditions. The hypothesis can be tested by specific intervention studies.

Breast Neoplasms↗
PubMed1994

Does early physical maturity influence breast cancer risk?

Earlier onset of menarche and tallness in adult women are mainly confirmed as risk markers for breast cancer. Recent disparate case-control studies have reported abdominal-type obesity and higher circulating levels of insulin, testosterone and insulin-like growth factor 1, to be further risk markers for breast cancer. There is evidence that abdominal-type obesity is recognisable in girls even before puberty, and disparate studies have shown it to be correlated with earlier onset of menarche, insulin resistance leading to hyperinsulinaemia, and an abnormal sex steroid profile. The implications are that earlier onset of puberty in a subset of girls can lead to more prolonged exposure of developing breast tissue to an abnormal sex steroid profile and also to a higher circulating level of insulin. It is postulated that these metabolic/endocrine concomitants of abdominal-type obesity could play a role in promoting mammary carcinogenesis at a young age, particularly if genetic predisposition is present.

Adolescent↗
PubMed1993

Can unorthodox cancer therapy improve quality-of-life?

The introduction of a psychosocial component into quality-of-life scores in cancer patients means that any belief which increases hope of cure on benefit will improve the score, and may override adverse physical components of the measurement. Such a belief may be the denial of a bad prognosis by some patients. There can be no objection to the patient seeking the temporary reassurance which may come from unorthodox therapies, as long as they are harmless and do not interfere with orthodox therapy. They may give the patient with a bad prognosis the necessary time to develop inner strengths enabling him to come to terms with the situation.

Complementary Therapies↗
PubMed1992

Spontaneous regression of cancer: new insights.

Suppression of oncogene expression and of host- or tumour-expressed growth factors and receptors may precipitate spontaneous regression or dormancy in human cancer. Loss of oncogenes necessary for progressive proliferation can lead to differentiation changes. Both natural factors and chemical agents can trigger such a change, and of the naturally occurring agents, growth factors and immunological factors have been most studied. We may find new clues to biological methods of prolonging arrest of cancer, by looking for cytogenetic abnormalities, alterations in oncogene expression and immunocytological composition, in patients showing prolonged dormancy of cancer.

Cell Differentiation↗