Radio Show Articles:
November 15, 2014

MM: Most diet programs fail in that they try to be rapid and tend to lose a predominance of muscle rather than fat thereby causing rapid return of weight and weight that is more fat than what was initially lost with the added problem of lowering overall metabolic rate. Other diets fail to train the person to establish viable lifelong tactics and habits that will deter future weight gain. The HCG Metabolic Syndrome approach deals with both of these problems. The weight lost is predominantly fat, not muscle and the lessons that are learned during the process tend to stay with patients for a long time as they progress. As the New Year approaches and resolutions to lose weight are made and broken, this is a great time to consider contacting your doctor or your Mark Drugs pharmacist about the HCG program options.

Popular Diets Achieve Only Modest Long-Term Weight Loss
By Larry Husten, Edited by David G. Fairchild, MD, MPH, and Lorenzo Di Francesco, MD, FACP, FHM
Four popular weight-loss diets produce at best only modest long-term benefits, with few differences across the four, according to a study in Circulation: Cardiovascular Quality and Outcomes.
Researchers examined 12 randomized, controlled studies of the Atkins, South Beach, Zone, or Weight Watchers diets. Ten studies compared one of the diets with usual care. In these, Weight Watchers was the only diet to consistently outperform usual care, but the difference in weight loss at 1 year was modest at best (range: 3.5-6.0 kg vs. 0.8-5.4 kg). In the two head-to-head trials, the Atkins and Zone diets resulted in a similar but modest weight loss. Longer-term data out to 2 years — available only for Weight Watchers and Atkins — indicated that some of the lost weight was regained over time.
An editorialist argues passionately that the focus on individual diets or specific macronutrients is misguided and unhelpful. He proposes a simple formula: "wholesome foods in sensible combinations."
http://circoutcomes.ahajournals.org/content/early/2014/11/11/
CIRCOUTCOMES.113.000723.abstract
Top of Page

MM: Although this study was performed on older women, the incidence in young women with depression and eating disorders tends to be rather substantial. many of these young women are vegetarians or vegans and vitamin B deficiency is not uncommon. This group needs to be more vigilant about their B complex supplementation that the typical public as do all patients with histories of depression.

Br J Psychiatry 2014 Sep 25
Can B Vitamins Enhance Antidepressant Response?
They might specifically prevent relapse in patients with antidepressant-remitted depression and improve response in those with elevated homocysteine levels
Folate and B12 deficiency can cause depression, and supplementation with methylfolate can augment short-term antidepressant response in nonresponders. In this randomized, controlled, 1-year study, 153 older, depressed patients (age, >50; 56% women) received citalopram (20–40 mg) plus either supplementation with placebo or with vitamins B6 (25.0 mg), B12 (0.5 mg), and folate (2.0 mg).
The vitamin and placebo groups did not differ in depression rating scale scores at 12, 26, or 52 weeks. However, among those whose depression remitted after week 12, supplementation was associated with a significantly lower relapse rate (odds ratio, 0.33). Vitamin supplementation also significantly reduced plasma level of homocysteine (which correlates negatively with intracellular vitamin B12 and folate levels). In a post hoc analysis of patients by baseline homocysteine levels, only patients with elevated levels (>10.4 µmol/L) showed greater odds of reaching remission at 52 weeks with supplementation than with placebo (OR, 3.47).
Comment: These results suggest that adding B6, B12, and folate to antidepressants is helpful to depressed elderly individuals who have biochemical evidence of a deficiency (elevated homocysteine). Supplementation may also help to prevent relapse in remitted patients. Therefore, in addition to standard testing for B12 and folate deficiency at baseline, clinicians should consider supplementation with B6, B12, and folate in all depressed patients, given the high tolerability and low cost of these vitamins
Citation(s): Almeida OP et al. B vitamins to enhance treatment response to antidepressants in middle-aged and older adults: Results from the B-VITAGE randomised, double-blind, placebo-controlled trial. Br J Psychiatry 2014 Sep 25; [e-pub ahead of print]. (http://dx.doi.org/10.1192/bjp.bp.114.145177)
Top of Page

MM: As the U.S. population encounters more challenges with obesity, the incidence of colorectal cancer tends to show a concomitant increase. This tendency may be applicable to other cancers as well. Starting with lifestyle modifications early is the best way to prevent a problem from developing later. In our practice, the HCG Weight Loss protocol has been successful with patients ranging from 16-86.

Colorectal Cancer Projected to Increase in Younger Adults
By Kelly Young, Edited by Susan Sadoughi, MD, and Richard Saitz, MD, MPH, FACP, FASAM
The incidence of colorectal cancer among U.S. adults younger than 35 is predicted to roughly double in the next two decades, according to a study in JAMA Surgery. (Low-risk adults typically don't begin colorectal cancer screening until age 50.)
Using cancer registries, researchers tracked trends in colon and rectal cancers from 1975 to 2010. They found an overall decrease in age-adjusted colorectal cancer. However, among adults aged 20 to 34, the incidence appeared to be increasing. By 2030, the researchers calculated, the incidence rates for colon and rectal cancers in this age group may increase 90% and 124%, respectively.
A commentator calls the results, "rather unsettling" while noting that the absolute risks for young adults are still quite low. He concludes: "This report should stimulate opportunities for development of better risk-prediction tools that might help us identify these individuals early and initiate better screening/prevention strategies."
http://archsurg.jamanetwork.com/article.aspx?articleid=1920838
Top of Page

MM: ALS is a degenerative disease where the body seems to be attacking its' own neuronal system. Low Dose Naltrexone (LDN) seems to modulate the immune system and has demonstrated some success with these patients. The problem with LDN is that it is off patent and too inexpensive to support large clinical trials. If I or a loved one had ALS, I would certainly consider LDN as an viable option or complementary treatment.

Lancet Neurol 2014 Nov; 13:1083
The Frustration of ALS Therapy Development
Another negative ALS clinical trial prompts a reappraisal of how we approach therapy development for this devastating neurodegenerative disorder.
In the search for potential treatments for amyotrophic lateral sclerosis (ALS), researchers previously identified ceftriaxone, a beta-lactam antibiotic that increases glutamate transporter activity, from a blinded screen of 1040 FDA-approved drugs and nutritionals based on expression of the glutamate transporter in rat spinal cord slice cultures. Validation studies included an assessment of preclinical efficacy in the SOD1 mouse model of ALS, showing prevention of motor neuron loss and prolonged survival. These data launched a multicenter clinical trial that proceeded in three stages. Based on pharmacokinetic (stage 1), and safety/ tolerability (stage 2) data, researchers now report findings from stage 3, in which 514 patients were randomized (2:1) to receive ceftriaxone 4 g/day or placebo, with the intent to continue treatment until the last enrolled patient completed 12 months of follow-up.
Ceftriaxone was found to offer no therapeutic benefit over placebo on the coprimary endpoints of survival (hazard ratio, 0.90; 95% CI 0.71–1.15) and rate of decline of the revised ALS functional rating scale (−1.13 points/month with ceftriaxone vs. −1.22 points/month with placebo), as well as on secondary endpoints (rate of decline of respiratory muscle and limb strength).
Comment: The million-dollar question in drug development for ALS is how to predict which agents are worthy of large, expensive phase-III clinical trials. Although based on sound science, this well-designed and effectively conducted clinical trial yielded disappointing results. One reason may relate to the recently highlighted problem of irreproducibility of preclinical science (Nature 2014 Jan 30; 505:612). Published data (albeit after initiation of this trial) show no effect of ceftriaxone in the SOD1 mouse model (Amyotrop Lateral Scler 2008 Jan; 9:4). Another possibility is that upregulation of glutamate transporter, aiming to mitigate glutamate excitotoxicity, may not be productive. The absence of a suitable pharmacodynamic biomarker of ceftriaxone's biological effect precludes such a conclusion. Trial results such as this are, appropriately, prompting a reappraisal of how we approach therapeutic development for ALS.
Citation(s): Cudkowicz ME et al. Safety and efficacy of ceftriaxone for amyotrophic lateral sclerosis: A multi-stage, randomised, double-blind, placebo-controlled trial. Lancet Neurol 2014 Nov; 13:1083.
(http://dx.doi.org/10.1016/S1474-4422(14)70222-4)

http://www.ncbi.nlm.nih.gov/pubmed/25297012?access_num=25297012&link_
type=MED&dopt=Abstract
Top of Page

MM: Many of us are fearful of developing Alzheimer's Disease (AD).What I liked about this article is that it actually establishes definitive guidelines of how much use of a specific drug and drugs within a class tends to predispose a person to a problem. The use of benzodiazepines such as Valium or Xanax is very common in society for anxiety or sleep problems. We tend to consider these drugs safe and well tolerated but the question of how safe they are, long term, arises and we become a little less cavalier in our opinions. It appears that quantity, frequency and duration of use appear to be the mast important factors regarding long term use and any time that we can minimize the use of these drugs, it would be an optimal approach.

BMJ 2014 Sep 9; 349:g5205
Benzodiazepine Use Might Raise Risk for Alzheimer Disease
In a case-control study, any use of these drugs from 5 to 10 years before AD diagnosis was associated with higher risk
Some evidence suggests that benzodiazepine use is associated with excess risk for dementia; however, benzodiazepines sometimes are prescribed for prodromes of dementia (e.g., anxiety, insomnia). In this case-control study, investigators examined the association between exposure to benzodiazepines and risk for developing Alzheimer disease (AD).Cases were 1800 randomly selected older community dwellers (age, >66) in Quebec who had received first diagnoses of AD and had been followed for at least 6 years before their AD diagnoses. Controls were 7200 similar residents who were matched to cases by age, sex, and duration of follow-up. To minimize reverse causality, only benzodiazepine exposure that occurred ≥5 years before diagnosis of AD was considered.
After adjustment for multiple variables (including anxiety, depression, and insomnia), any benzodiazepine use (compared with nonuse) was associated with excess risk for AD (odds ratio, 1.5). Cumulative exposure to 1 to 90 prescribed daily doses (PDDs) of benzodiazepines was not associated with excess risk, but exposure to 91 to 180 PDDs (OR, 1.3) and >180 PDDs (OR, 1.7) were. The association was stronger for long-acting benzodiazepines (OR, 1.6) than for short-acting benzodiazepines (OR, 1.4).
Comment: Researchers carefully controlled for reverse causality and potential confounders and found that benzodiazepine use was associated with excess risk for AD. The authors note that chronic benzodiazepine use induces a downregulation of binding receptors and that a reduction in the number of these receptors is correlated with cognitive decline.
Citation(s): Billioti de Gage S et al. Benzodiazepine use and risk of Alzheimer's disease: Case-control study. BMJ 2014 Sep 9; 349:g5205.
(http://dx.doi.org/10.1136/bmj.g5205)

http://www.bmj.com/content/349/bmj.g5205?ijkey=5af4af50ea4ed07cc7acfa5fadf36d7da49c
be06&keytype2=tf_ipsecsha
Top of Page

MM: As a person ages it becomes a more poignant question of how much extended life is desirable and at what monetary and Quality of Life (QOL) cost life should be extended. This article addresses this issue in an indirect way. If a person is being treated for cancer, do we truly have to be overly concerned with their cholesterol? It's sort of like giving a condemned person their choice of a last meal. We don't really care whether the food is healthy or detrimental as this takes a back seat to the eminent demise of the person. If a cholesterol medication causes increased pain in an elderly cancer patient, why are we administering it?

J Am Geriatr Soc 2014 Oct; 62:1900
Statins and Pain in Older Cancer Patients
In patients older than 80, statin use was associated with higher odds of general pain.
Determining whether statins are responsible for nonspecific aches and pains can be difficult, especially in elders. Australian researchers explored this association in a cohort of 385 older cancer patients (age, ≥70) who were referred to a geriatric oncology outpatient unit. Half the patients were referred for palliative care, 36% were taking statins, and half the statin use was for primary prevention.
Self-reported general pain was assessed on a 10-point visual analog scale. In the oldest patients (age, ≥80), having a pain score ≥5 was associated significantly with statin use (odds ratio, 4.1), after adjustment for variables including age, comorbidities, and analgesic use. In the younger group (age range, 70–79), no significant association was observed.
Comment: Two points emerge from this study. First, many older cancer patients were receiving statins — often for primary prevention. This observation suggests therapeutic inertia, in which clinicians fail to stop unnecessary medications; indeed, it's not clear that statins should be prescribed for primary prevention even in 80-year-old patients without cancer. Second, although this study doesn't prove causality, it supports the clinical impression of many clinicians that older patients are especially prone to musculoskeletal side effects of statins.
Citation(s): Turner JP et al. Statin use and pain in older people with cancer: A cross-sectional study. J Am Geriatr Soc 2014 Oct; 62:1900.
(http://dx.doi.org/10.1111/jgs.13051)

http://www.ncbi.nlm.nih.gov/pubmed/25284040?access_num=25284040&link_
type=MED&dopt=Abstract
Top of Page

MM: We normally expect low impact exercise to be an optimal form but it appears that in young girls, with developing skeletons, an unnatural forced positioning of the spine may be detrimental.

AJ Pediatr 2014 Oct 24
Competitive Swimming Is Associated with Spinal Deformities in Girls
Risks for trunk asymmetries and lower back pain were more than doubled in girls but not in boys.
Although its efficacy is unproven, swimming has been recommended as an acceptable exercise, and possibly a potential treatment, for children and adolescents with spinal deformities.
To further investigate this issue, researchers compared the prevalence of spinal deformities in a convenience sample of 112 competitive swimmers (mean age, 12.5 years; 62 girls) and 217 adolescents from public schools (controls) in Italy. Swimmers trained for 2 to 2.5 hours at least 4 times weekly. Participants were evaluated for spinal deformities using a scoliometer and completed a questionnaire to assess lower back pain.
No differences in trunk rotation were found between boys who swam and controls. Girls who swam had a 2.5-fold elevated risk for trunk deformities. Swimming was associated with greater than 2-fold elevated risks for hyperkyphosis and hyperlordosis in both boys and girls. Swimming was associated with a 2-fold elevated risk for lower back pain in girls but was not associated with lower back pain risk in boys.
Comment: These data suggest that swimming might not be an effective treatment for spinal deformities in girls and might even be detrimental. Swimming should not be recommended for adolescent girls with scoliosis. Unfortunately, the cross-sectional study design could not exclude the possibility that participants had spinal deformities before they began swimming.
Citation(s): Zaina F et al. Swimming and spinal deformities: A cross-sectional study. J Pediatr 2014 Oct 24; [e-pub ahead of print].
(http://dx.doi.org/10.1016/j.jpeds.2014.09.024)
Top of Page

MM: As a new grandparent I keep my eyes open for unsuspected infant and toddler dangers. Perhaps I am overly sensitive to these things but apparently, I'm not the only one.

Pediatrics 2014 Nov; 134:e1293
Why Sofa Sleeping Is Deadly for Infants
Unexpected infant deaths on sofas were twice as likely to be from accidental suffocation and strangulation as deaths on beds or cribs.
The incidence of sudden infant death syndrome (SIDS) has declined more than 50% since the national “Back to Sleep” campaign was launched in 1992, while the incidence of other sleep-related infant deaths (accidental suffocation, strangulation, ill-defined causes) has not declined and may have increased. Sleeping on a sofa has been shown to increase the risk for infant death at least 50 times compared with sleeping on other surfaces (e.g., beds, cribs). To determine what makes sleeping on a sofa so hazardous, researchers analyzed a database of infant deaths in 24 states from 2004 to 2012.Of 7934 sleep-related deaths, 1024 occurred on sofas and 6910 on other surfaces. Deaths on sofas were twice as likely to be classified as accidental suffocation or strangulation. Infants who died on sofas were less likely to be Hispanic and to be in an environment where other objects were present. They were more than twice as likely to be sharing the surface with another person, twice as likely to be found on their sides, and more than 6 times as likely to not be in their usual sleep location. Infants who died on sofas were more likely to have had prenatal smoke exposure.
Comment: That sofas can be deadly sleep surfaces to infants is inherent to their design (soft cushions, a downward slope to the back cushion) and function (sharing). The temptation to lie down with one's infant for a brief rest on the sofa can be deadly and should be avoided. At the first visit, along with the “back to sleep” advice, parents should be given anticipatory guidance warning them of the dangers of sofa sleeping.
Citation(s): Rechtman LR et al. Sofas and infant mortality. Pediatrics 2014 Nov; 134:e1293. (http://dx.doi.org/10.1542/peds.2014-1543)

http://pediatrics.aappublications.org/content/134/5/e1293?ijkey=
b9ce478c137281b2c9c0972382ae4ae3824f2354&keytype2=tf_ipsecsha
Top of Page

MM: Humans are the only species that consumes the lactation of another species. We may like the taste but must also accept that there may be an inherent risk in consumption. Like so many other things in life, excessive quantities may be a problem..

BMJ 2014 Oct 28; 349:g6015
Is There Such a Thing as Too Much Milk?
In a Swedish observational study, high milk consumption was associated with excess risks for fractures and death.
Dairy products are promoted to lower fracture risk. However, milk contains d-galactose, which induces oxidative stress and chronic inflammation in animal models and, thus, might have deleterious long-term health effects. In this observational study of 61,000 women and 45,000 men who completed food-frequency questionnaires, Swedish investigators assessed whether high milk consumption is associated with excess risk for fractures and death.
During a mean follow-up of 20 years, women who drank ≥3 glasses of milk daily (compared with those who drank <1 glass) had higher risks for all-cause death (adjusted hazard ratio, 1.9), cardiovascular-related death (HR, 1.9), cancer-related death (HR, 1.4), any fracture (HR, 1.2), and hip fracture (HR, 1.6); significant dose-response relations were observed. During a mean follow-up of 11 years, men who drank ≥3 glasses of milk daily had higher risks for all-cause death (HR, 1.1) and cardiovascular-related death (HR, 1.2). Milk consumption was associated positively with elevated urinary and serum levels of biomarkers for oxidative stress and inflammation in both sexes. However, consumption of cheese and fermented milk products (e.g., yogurt) was not associated with these effects.
Comment: These authors theorize that d-galactose accounts for the excess risks for death and fracture associated with high milk consumption. This theory is supported by the observation that consuming cheese and fermented milk products — which do not contain d-galactose — was not associated with such negative health effects. Thus, although the authors cannot rule out the possibility of residual confounding and reverse causation, perhaps milk is not a magic bullet.
Citation(s): Michaëlsson K et al. Milk intake and risk of mortality and fractures in women and men: Cohort studies. BMJ 2014 Oct 28; 349:g6015.
(http://dx.doi.org/10.1136/bmj.g6015)

http://www.bmj.com/content/349/bmj.g6015?ijkey=a0696e251eae88aad1e2ad1acaaa3
4359639a78f&keytype2=tf_ipsecsha
Top of Page

MM: It has been reported that there are several potentially effective vaccines and treatment protocols for Ebola. All should be investigated and reviewed in the event that there is a legitimate answer. The ethical question of whether a patient should receive a placebo is, in my opinion, no. A patient should not receive a placebo if they are at certain risk of death. However, I am not opposed to having patients challenged with alternative treatments. Since the presence of a single agent is rarely the case, it would seem to me that there exist several alternatives and that is a better way to see which has the greatest survival/success qualities. This is an ethical approach but the potential problem is that one may be established as more effective than another if the playing field is level and that means that someone will have a big pay day and someone may not. Once again, we see greed standing in the way of effective medical treatment.

Ebola Treatment Clinical Trials and Placebos
TFDA Assistant Commissioner Dr. Luciana Borio is troubled by European Ebola-trial plans that lack a placebo group. A European consortium, made up of European universities and medical groups, plans to give experimental drugs to West African Ebola patients without assigning some to a placebo group; this has touched off an intense trans-Atlantic quarrel over what is ethical and effective in treating the virus.
The academic and medical groups in the U.K. and France, the Wellcome Trust, Doctors Without Borders, and Institut Pasteur of France, have decided to give the drugs to sick African patients without randomly assigning other patients to a control group not getting the medicines. The rationale is that in a ghastly epidemic, it is unethical to hold back treatment from anyone. This has put them at odds with senior US officials at the FDA and NIH in the US.
http://online.wsj.com/articles/plan-to-offer-ebola-drugs-without-clinical-trials-draws-fire-1414713563
Top of Page

MM: Is the Ebola threat in the United States gone? This question remains unanswered but is most likely "No!" As long as there is a threat in the world of this deadly disease, and people continue to travel around the world, there will be a threat.

Ebola Monitoring of Texas Contacts Ends Friday
The 21-day monitoring period for people who were connected with one of three Ebola patients in Texas ends Friday night, according to the Texas Department of State Health Services. So far, no one else in Texas has contracted Ebola beyond the original case from Liberia and two of his nurses.
In total, 177 healthcare workers, household contacts, and people in the community had their temperature and symptoms monitored regularly because they had contact with one of the three patients, specimens, or medical waste. The last person to pass the 21-day mark (the end of Ebola's incubation period) is a worker who handled medical waste on Oct. 17.
http://www.dshs.state.tx.us/news/releases/20141106.aspx
http://www.nejm.org/page/ebola-outbreak
Top of Page

MM: The answer that we typically associate with why generic drug prices are increasing is typically associated with injectible drugs. The reason behind this is supposed to be that as generics came on the market, the demand for the more expensive brand names dried up. This caused the brands to essentially disappear. When the generic manufacturers of sterile products had their manufacturing plants inspected and challenged RE quality and sterility, then the supply became diminished so the prices went up due to a constant demand and the alleged costs of making those manufacturing plants compliant with the standards necessary to safely produce those products. This argument fails to hold water with non-sterile dosage forms and the bottom line is that the generic manufacturers have decided that they want a bigger piece of the healthcare pie. The bottom line is greed in lieu of production. major drug manufacturers have a 20-42% Net profit. Generic manufacturers have typically shown a 8-12% net profit. Just follow the numbers.

Why Are Generic Drug Prices Increasing?
Originally, generic drugs were supposed to save Americans millions of dollars, but today some cost as much or more than brand-name drugs. The increase in prices has some congressmen shocked, and they're joining doctors, pharmacists, and patients in asking why. Examples include two generic drugs, including Simvastatin for high cholesterol and amlodipine for high blood pressure, with an increase in total cost that has tripled from $45 to $140 per month; an ointment for eczema and psoriasis is another example which used to cost $10 for an entire tube and now costs $300.
http://chicago.cbslocal.com/2014/10/31/prices-soar-for-some-generic-drugs-why/
Top of Page

MM: If you fail to play by the rules and hurt someone then you will inevitably have to pay the price. A sad aspect of this is that this failure in providing a quality production environment is not limited to overseas locations. Morton Grove is a near northwest suburb of Chicago and a little too close to home.

India's Drug Company Profit Plunges from US Export Bans
Wockhardt Ltd., an Indian generic drugmaker, reported a 97% drop in quarterly net profit, as regulatory bans on the company's manufacturing plants in India due to poor production processes hit sales in the US, its largest market. Last year, the US FDA banned two of Wockhardt's major manufacturing plants from exporting to the US after finding manufacturing quality violations there. Also, in May of this year, Wockhardt said the FDA had also expressed concerns over production processes at its Chicago-based Morton Grove Pharmaceuticals unit, which accounts for more than 50% of Wockhardt's sales in the US.
http://www.reuters.com/article/2014/11/03/wockhardt-results-idUSL4N0ST36220141103
Top of Page

MM: Knowing the actual risks and then being able to test for those risk factors is a good way of determining if a person needs to be concerned about a potential danger and also determines how much concern is necessary. Testing at risk patients makes sense but testing low risk patients may not. It all depends on the severity of the consequences and the quality and cost of the testing. And, finally on the success of the treatment. It does little good to know something if you can't do much about it.

J Natl Cancer Inst 2014 Oct; 106:dju237
Black Women, Breast Cancer, and Lactation
Mothers who don't breast-feed are at increased risk for aggressive breast cancer
Breast cancers lacking estrogen receptors (ER−) carry a worse prognosis and are more common among black women in the U.S. To examine the relation between parity, lactation, and breast cancer subtypes, investigators for the African American Breast Cancer Epidemiology and Risk (AMBER) consortium analyzed data pooled from 4 studies including 3698 black women with breast cancer and 14180 without breast cancer.
In both unadjusted and multivariable analyses, risk for ER+ breast cancer was not affected by parity, but risk for ER− breast cancer increased with each additional birth among mothers who had not breast-fed. Overall, lactation did not affect risk for ER+ cancer but was associated with a 19% reduction in risk for ER− breast cancer.
Comment: Weaning is hypothesized to result in gradual involution of breast tissue, whereas not breast-feeding is associated with more-abrupt activation of fibroblasts and an influx of tumorigenic cells. Although findings similar to those of this study were previously reported in a predominantly white population, these results confirm that disparities in access to lactation support (as well as employment environments that enable mothers to pump while working outside the home) seem directly linked to persistent disparities in breast cancer morbidity and mortality in the U.S. (NEJM JW Womens Health Sep 23 2014).
Citation(s): Palmer JR et al. Parity, lactation, and breast cancer subtypes in African American women: Results from the AMBER Consortium. J Natl Cancer Inst 2014 Oct; 106:dju237. (http://dx.doi.org/10.1093/jnci/dju237)

Top of Page

Radio Show Articles: November 15, 2014

Radio Show Articles:
November 15, 2014