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Biomedical subjects

V Herbert

Publications and source records attributed to V Herbert.

At least 73 records · Page 4Linked to original sources
PubMed1987

Recommended dietary intakes (RDI) of folate in humans.

Extensive evidence is presented that 3 micrograms folate/kg (6.8 nmol/kg) body weight daily will not only maintain adequate folate nutriture but also a substantial reserve body pool in normal persons. Recommendations appropriate to this extensive evidence are presented.

Adolescent↗
PubMed1987

Recommended dietary intakes (RDI) of vitamin B-12 in humans.

Extensive evidence is presented that 2 micrograms (1.5 nmol) of cobalamin daily will not only maintain adequate vitamin B-12 nutriture but also a substantial reserve body pool in normal persons. Recommendations appropriate to this extensive evidence are presented.

Adolescent↗
PubMed1987

Recommended dietary intakes (RDI) of iron in humans.

Evidence is presented that requirements for dietary iron must take into account increasing percentage absorbability of iron from plant foods as quantity of iron in such foods decreases and, also, toxicity of iron. Recommendations appropriate to this evidence are presented.

Adolescent↗
PubMed1986

Unproven (questionable) dietary and nutritional methods in cancer prevention and treatment.

"Unproven" is a euphemism for questionable. The definition of a questionable method is that it has not successfully answered the two basic consumer protection questions of efficacy and safety, to wit: Has it been responsibly, objectively, reproducibly, and reliably demonstrated in humans in the responsible (peer-reviewed) literature accepted for the shelves of the National Library of Medicine in Bethesda, Maryland, to be: More effective than suggestion or doing nothing? and in addition, either As safe as doing nothing? or, in the alternative, If there is any question with respect to safety, to have a reasonably and objectively clear potential for benefit which exceeds its potential for harm? Any proposed cancer prevention or treatment modality which has not successfully answered the above efficacy question plus one of the two safety questions is by definition questionable. It is experimental if it is new, and very probably quackery if it is old. Experimental therapy may be either ethical and responsible or unethical and irresponsible. It is unethical and irresponsible to not tell the patient experiments are being conducted on him, to charge the patient to perform research on him, or to ask the patient to sign an informed consent aimed at exculpating the doctor rather than protecting the patient. Ethical and responsible informed consents clearly delineate that what is being done is experimental, and that efficacy and safety have not been determined. Products promoted for profit to the public without passing peer process are almost without exception ineffective, often harmful, and sometimes lethal. This includes Laetrile, immunoaugmentative therapy, chelation therapy, macrobiotic diets, and other alternative therapies. Anecdotal and testimonial claims of cure, on investigation, almost invariably prove due to coincidence, suggestibility, and/or the natural history of the disorder, and fall into one of the five categories of "cures that are not": The patient never had cancer. The cancer was cured or put in remission by responsible therapy, but the promoted therapy was irrelevantly also given, and is erroneously credited for the cure. The cancer is progressing silently, but erroneously represented as cured. The patient is dead, but represented as cured. The patient had a spontaneous remission, which is publicized as a "cure," while failing to publicize the hundred or more deaths per "success" which followed the same "cure." Quackery involves the consumer fraud of taking money under false pretenses. The false pretense is the promotion and selling of questionable diagnostic tests and therapies advertising them to be safe and effective.(ABSTRACT TRUNCATED AT 400 WORDS)

Complementary Therapies↗
PubMed1986

The role of vitamin B12 and folate in carcinogenesis.

The roles of vitamin B12 and folate in carcinogenesis are largely extensions of and linked to their roles in normal metabolism, particularly 1-carbon unit metabolism. A possible key area may be hypomethylation to "switch on" genes and methylation to "switch them off." Some vitamin analogues may act as antivitamins in these reactions, as may some vitamin-binding proteins. Others may act as specific delivery proteins. Using appropriate radioactive substrates and suspensions of vitamin-dependent normal and malignant cells, it may be possible to work out their positive and negative control of DNA synthesis.

Carcinogens↗
PubMed1986

Detection of folate deficiency in alcoholism using the peripheral blood lymphocyte deoxyuridine suppression test.

Twenty-seven alcoholic patients were studied for folate status. Twenty-two (81%) had neutrophil hypersegmentation and were detected as folate deficient by also having low serum folate, erythrocyte folate, lymphocyte folate and/or an abnormal peripheral blood lymphocyte deoxyuridine suppression test. Seventeen (63%) had an abnormal lymphocyte deoxyuridine suppression test and all 17 were corrected by the addition of methyltetrahydrofolate or pteroylglutamate. Comparison of these 63% abnormal (corrected by folate) results using the peripheral blood lymphocyte deoxyuridine suppression test with the lower percent abnormal (corrected by folate) bone marrow deoxyuridine suppression tests found in folate-deficient alcoholics by others suggests that the peripheral blood deoxyuridine suppression test may be more useful than the bone marrow deoxyuridine suppression test for laboratory diagnosis of folate deficiency responsive to folate therapy in alcoholism. Hidden iron deficiency is common in alcoholism, and in the concomitant presence of deficiencies of hemoglobin synthesis and of folate, the serum and erythrocyte folate and deoxyuridine suppression test in bone marrow are frequently normal, despite the suppression test being abnormal in lymphocytes and corrected by folate.

Adult↗
PubMed1986

Rapid collection of human intrinsic factor uncontaminated with cobalophilin (R binder).

Intrinsic factor and R binder cobalamin binding capacity (CblBC) were measured in gastric juices obtained through feeding gastrostomy tubes (FG-GJ) from six patients with relatively complete obstruction to swallowing because of surgical resections for oropharyngeal or laryngeal carcinomas. Controls were six nonpernicious anemia gastric juices. In five of the six FG-GJ 97% of CblBC was intrinsic factor. In the sixth FG-GJ, with GJ pH = 7.2, in addition to intrinsic factor there was 22% nonintrinsic factor cobalamin-specific binder, which presumably represented partially degraded R binder refluxed from the duodenum. These data demonstrate that relatively "pure" intrinsic factor, i.e., uncontaminated with other cobalamin binders, can easily be obtained by simple drainage of FG-GJ. The study also supports evidence that gastric juice R binder is either swallowed or refluxed from the duodenum, and does not originate in the stomach.

Gastric Juice↗
PubMed1985

The effect of raw wheat bran, alfalfa meal and alpha-cellulose on iron ascorbate chelate and ferric chloride in three binding solutions.

Iron ascorbate chelate was prepared and purified with iron and ascorbate combined in a 1:1 molar ratio. Some iron dissociated from the chelate and bound to raw wheat bran and alfalfa meal, indicating something in these fiber sources produced the dissociation. The chelate bound intact to alpha-cellulose in bicarbonate and phosphate buffer. More iron as ferric chloride bound to the three fiber sources than did iron as chelate. Iron became more soluble in bicarbonate buffer in the presence of raw wheat bran and alfalfa meal, but became less soluble in phosphate buffer in the presence of these fiber sources.

Ascorbic Acid↗
PubMed1985

Cobalamin-specific R binder in pernicious anemia gastric juice: production by digestive enzyme action on saliva R binder.

We found in four of five pernicious anemia gastric juices a partly degraded R binder which was cobalamin specific and has an apparent molecular weight of 60-70,000 daltons. Twenty-nine to 74% (4.8-27.0 ng/ml) of the corrinoid binding capacity could not be blocked by cobinamide (a noncobalamin corrinoid). The fifth pernicious anemia gastric juice and five nonpernicious anemia gastric juices had minimal amounts of this binder (2.5 and 2.2 +/- 1.4 ng/ml). Scatchard analysis revealed that cobalamin-specific R binder has 1000-fold lower affinity for cobinamide than cobalamin. Increasing quantities of trypsin and/or chymotrypsin digested increasing amounts of saliva R binder and an increasing percentage of the remaining digest-resistant R binder acquired cobalamin specificity. Partly degraded R binder in pernicious anemia gastric juice was resistant to further proteolysis. Cobalamin-specific R binder, perhaps produced in vivo by the action of refluxed pancreatic enzymes on swallowed R would preferentially bind ingested and/or biliary cobalamin rather than analogue and thereby could play a role in hastening the development of cobalamin deficiency in pernicious anemia.

Anemia↗
PubMed1985

Enhancement by human bile of the binding of free and intrinsic factor-bound cobalamin (vitamin B12) to small bowel epithelial cell receptors.

The effect of human bile on the binding of free cobalamin (Cbl) and of intrinsic factor-Cbl (IF-Cbl) complexes to intestine receptors was examined in in vitro receptor extracts made from guinea pig small bowel epithelial cells. Cbl and IF-Cbl complex binding to the receptors was measured in the effluent from a Sephadex G-200 column. Intrinsic factor-Cbl binding to the receptors in the control samples was 4.32 +/- 0.07 ng/animal (mean +/- SEM); addition of bile, saturated with excess 57Co-Cbl enhanced binding to 5.26 +/- 0.16 ng/animal (p less than 0.001). These data suggest that bile enhances binding of IF-Cbl complex onto ileal receptors. Whether bile also serves as "releasing factor" by releasing Cbl from intrinsic factor in vivo remains to be determined.

Animals↗
PubMed1985

Total corrinoid, cobalamin (vitamin B12), and cobalamin analogue levels may be normal in serum despite cobalamin in liver depletion in patients with alcoholism.

Serum, erythrocyte, and liver levels of total corrinoids, cobalamin (vitamin B12), and cobalamin analogues were determined by differential radioassay in 27 patients with alcoholism. Compared with normal subjects, liver content of total corrinoids and cobalamin in alcoholics was low. Conversely, serum total corrinoids and cobalamin were high. Compared with normal, levels of erythrocyte cobalamin analogue in alcoholics were elevated, but levels of cobalamin were not. Analogues in liver represented a similar percentage of total corrinoids in alcoholics as in normals. The data confirm prior work suggesting that, in alcoholism and in liver disease, cobalamin depletion in tissues may be masked by normal to high serum cobalamin and analogue levels. The failure of damaged liver to take up from the serum cobalamin and analogues, compounded by release of these compounds and their binders from damaged liver into the serum, can account for these findings.

Adult↗