Reposted from TS Wiley's newsletter: What Can Your Patients Do To Protect Against Breast Cancer if they are BRCA1 Carriers

What can your Patients do to Protect against Breast Cancer if they are BRCA1 Carriers?

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T.S. Wiley is and always will be a strong proponent of breastfeeding babies into toddler hood, primarily as the single strongest action against preventing breast cancer.

In her book, "Sex, Lies and Menopause", she notes the "collaborative reanalysis of individual data" published in July 2002 in the Lancet, from 47 studies in 30 countries, including 50,302 women with breast cancer and 96,973 women without the disease. "Researchers concluded that if women in developed nations like the United States breast fed nine months longer than the norm, which is three months, breast cancer deaths would be reduced by 25,000 lives. Furthermore, and most importantly, if women breast fed twelve months longer, or fifteen months in total, as is the norm in developing nations, lives saved from breast cancer each year would approach 50,000. Since only about 47,000 of us are expected to die from breast cancer this year, that's all of us who would be saved".
Introduction

Breastfeeding has been inversely related to breast cancer risk in the general population. Clarifying the role of breastfeeding among women with a BRCA1 or BRCA2 mutation may be helpful for risk assessment and for recommendations regarding prevention. We present an updated analysis of breastfeeding and risk of breast cancer using a large matched sample of BRCA mutation carriers.
Methods

We conducted a case-control study of 1,665 pairs of women with a deleterious mutation in either BRCA1 (n = 1,243 pairs) or BRCA2 (n = 422 pairs). Breast cancer cases and unaffected controls were matched on year of birth, mutation status, country of residence and parity. Information about reproductive factors, including breastfeeding for each live birth, was collected from a routinely administered questionnaire. Conditional logistic regression was used to estimate the association between ever having breastfed, as well as total duration of breastfeeding, and the risk of breast cancer.
Results

Among BRCA1 mutation carriers, breastfeeding for at least one year was associated with a 32% reduction in risk (OR = 0.68; 95% CI 0.52 to 0.91; P = 0.008); breastfeeding for two or more years conferred a greater reduction in risk (OR = 0.51; 95% CI 0.35 to 0.74). Among BRCA2 mutation carriers, there was no significant association between breastfeeding for at least one year and breast cancer risk (OR = 0.83; 95% CI 0.53 to 1.31; P = 0.43).
Conclusions

These data extend our previous findings that breastfeeding protects against BRCA1-, but not BRCA2-associated breast cancer. BRCA mutation carriers should be advised of the benefit of breastfeeding in terms of reducing breast cancer risk.
Introduction

In the general population, reproductive factors, including late age at menarche, parity and breastfeeding, have been shown to protect against the development of breast cancer. Various proposed mechanisms include reducing lifetime exposure to ovarian hormones, reducing the cumulative number of ovulatory cycles and differentiation of the breast lobules. We and others have evaluated the impact of reproductive factors in the etiology of BRCA-associated breast cancer, although the results are conflicting and vary by BRCA1 or BRCA2 mutation. With respect to breastfeeding and breast cancer risk in BRCA1 mutation carriers, two previous studies reported no relationship and three studies reported a protective effect. One case-control study of BRCA2 mutation carriers reported no association between breastfeeding and breast cancer risk.

We have previously reported in a study of 965 matched pairs that the total duration of breastfeeding was associated with a significant reduction in breast cancer risk among BRCA1, but not among BRCA2, mutation carriers. The association was particularly strong for breastfeeding for more than one year (OR = 0.55; 95% CI 0.38 to 0.80). No association was seen for BRCA2 mutation carriers (OR = 0.95; 95% CI 0.59 to 1.59). Here we update the analysis of total duration of breastfeeding and risk of breast cancer using a larger sample of BRCA mutation carriers with the addition of 700 matched pairs. Because childbirth and breastfeeding are strongly correlated, we restricted the present analysis to parous women and we matched on parity to eliminate any potential confounding effect of parity.
Methods
Study population

Eligible study subjects were identified at one of 62 participating centers in seven countries. These women were participants in ongoing research protocols at the host institutions. These women sought testing for BRCA1 and BRCA2 mutations because of a personal and/or family history of breast and/or ovarian cancer. All study subjects, (with the exception of some participants from the research study of SLN), received genetic counselling. The institutional review boards of the host institutions approved the study. All subjects provided written informed consent. In most cases, testing was initially offered to women who had been previously diagnosed with breast or ovarian cancer. When a BRCA1 or BRCA2 mutation was identified in a proband or her relative, genetic testing was offered to other at-risk individuals in the family. Mutation detection was performed using a range of techniques, but all nucleotide sequences were confirmed by direct sequencing of DNA. A woman was eligible for the current study when the molecular analysis established that she was a carrier of a deleterious mutation in the BRCA1 or BRCA2 gene.
Data collection

All study subjects completed a baseline questionnaire at the individual center at the time of a clinic appointment or at their home at a later date. The questionnaire requested information on family and personal history of cancer, reproductive and medical histories, including preventive oophorectomy and mastectomy. Detailed information regarding ages at menarche and menopause, cause of menopause, pregnancy, breastfeeding history, and hormone use was also queried. For each live birth, women were asked to recall how long they breastfed each child and to indicate the number of months of breastfeeding. We estimated the total duration of breastfeeding for each woman by summing the months of breastfeeding for each live birth.
Case and control subjects

Information on cancer status was available for a total of 12,116 women who carried a BRCA1 or BRCA2 mutation. Case subjects were women with a diagnosis of invasive breast cancer. Control subjects were women who never had breast cancer and who were also carriers of a mutation in BRCA1 or BRCA2. Potential subjects were excluded if they were nulliparous (n = 2,626) or if information on parity (including year of last birth) was missing (n = 320), if they had been diagnosed with ovarian or other cancer (n = 2,325), if information on breastfeeding was missing (n = 721), if BRCA mutation status was missing (n = 191) or if other pertinent information was missing (n = 54). After exclusions, there was a total of 5,879 eligible women, including 2,784 women with breast cancer (potential case subjects) and 3,095 women without breast cancer (potential control subjects).

A single control subject was selected for each case subject, matched according to mutation in the same gene (BRCA1 or BRCA2), year of birth (within one year), country of residence (Poland, USA, Canada, Israel, Austria, Italy, United Kingdom), and parity (number of births). We only included live births one or more years prior to the breast cancer diagnosis of the case for both the cases and controls. A control was eligible to be matched to a given case if the date of interview or date of prophylactic mastectomy in the matched control occurred at or after the year of breast cancer diagnosis of the case and if the last live birth of the control was at least one calendar year prior to the year of breast cancer diagnosis of the case. In total, 1,665 matched sets were identified. An appropriate match could not be located for 1,119 of the eligible cases because the date of birth of these cases (mean year of birth 1947.99; range 1901 to 1981) was substantially earlier compared to the pool of remaining controls (mean year of birth 1966.57; range 1903 to 1989).
Statistical analysis

A matched case-control analysis was performed to evaluate the association between breastfeeding and the risk of breast cancer. We censored breastfeeding one year prior to the diagnosis of the matched case. The distributions of continuous and categorical variables between cases and controls were compared using the Student's t-test and chi-square test, respectively. Conditional logistic regression was used to estimate the univariate odds ratios (OR) and 95% confidence intervals (CI) for breast cancer associated with breastfeeding (ever/never) and total duration of breastfeeding (months). A multivariate analysis was carried out to control for potential confounders. All analyses were performed using the SAS statistical package, version 9.1.3 (SAS Institute, Cary, NC, USA). All P-values were based on two-sided tests and were considered statistically significant if P ≤ 0.05.
Results

Case and control subjects were similar with respect to year of birth, oral contraceptive use, age at last birth, smoking status and body mass index (BMI) at age 30 (Table 1). Cases with a BRCA1 mutation had a significantly earlier age at menarche than controls (13.09 years vs. 13.27 years; P = 0.003) and were less likely to have consumed alcohol (61% vs. 67%; P = 0.002). Although not significant, age at first birth (24.8 vs. 25.1; P = 0.08) and age at last birth (29.0 vs. 29.3; P = 0.06) were, on average, earlier in BRCA1 mutation carriers compared with controls. Hormone replacement therapy (HRT) use was significantly lower in both BRCA1 and BRCA2 cases versus controls (5% vs. 12%; P < 0.0001 and 10.7% vs. 16.5%; P = 0.02, respectively). Age at menarche, age at first birth, age at last birth, mean duration of breastfeeding and alcohol consumption did not differ between cases and controls with a BRCA2 mutation.

Table 1. Baseline characteristics of breast cancer cases and controls with BRCA1 and BRCA2 mutations.

The mean duration of breastfeeding was shorter among the cases than the controls with a BRCA1 mutation (8.8 months vs. 10.4 months; P = 0.0009). There was a significant reduction in breast cancer risk with breastfeeding among women with a BRCA1 but not a BRCA2 mutation (Table 2). On average, BRCA1 cases breastfed for 1.6 fewer months than controls (8.8 vs. 10.4 months P = 0.0009). There was only a 0.5-month difference between cases and controls with a BRCA2 mutation (10.2 vs. 9.7 months P = 0.56). Among BRCA1 mutation carriers, breastfeeding for at least one year was associated with a 32% reduction in risk (OR = 0.68; 95% CI 0.52 to 0.91; P = 0.008); breastfeeding for two or more years conferred an even stronger reduction in risk (OR = 0.51; 95% CI 0.35 to 0.74; P = 0.0003). Each year of breastfeeding conferred a 19% reduction in risk. The effect of breastfeeding was present for women diagnosed at all ages. The reduction in risk associated with breastfeeding for one or more years compared with never breastfeeding was 44% for women with an age at breast cancer diagnosis of ≤ 39 (OR = 0.56; 95% CI 0.33 to 0.96), 54% for those with an age at diagnosis of 40 to 49 (OR = 0.46; 95% CI 0.26 to .81) and 69% for those with an age at diagnosis of ≥ 50 (OR = 0.31; 95% CI 0.07 to 1.30).

Table 2. Relationship between duration of breastfeeding and risk of breast cancer among BRCA1 and BRCA2 mutation carriers.

Among BRCA2 mutation carriers, there was no significant association between breastfeeding for at least one year and breast cancer risk (OR = 0.83; 95% CI 0.53 to 1.31; P = 0.43). There was no relationship following stratification by age at diagnosis. The risk estimates associated with breastfeeding for one or more years compared with never breastfeeding by age at diagnoses ≤ 39, 40 to 49 and ≥ 50 were 0.98 (95% CI 0.37 to 2.62), 1.41 (95% CI 0.59 to 3.43) and 0.91 (95% CI 0.24 to 3.43), respectively.
Discussion

The goal of the current study was to evaluate the relationship between breastfeeding and breast cancer risk among women with a BRCA1 or BRCA2 mutation. Because of the strong relationship between parity and breastfeeding, we limited our analysis to parous women and we matched cases and controls on parity. Here we report that ever having breastfed and the total duration of breastfeeding conferred substantial reductions in breast cancer risk among BRCA1, but not BRCA2 mutation carriers. Breastfeeding for one or more years conferred a significant 32% reduction in risk in BRCA1 mutation carriers. These findings are in agreement with our earlier publication, which was based on a subset of these women. In the present study, we expand our study sample from 995 to 1,665 matched pairs and we have matched on parity. The current study provides the most up-to-date evaluation of this association and should be helpful for genetic counsellors. The current study pertains to women who choose not to have a bilateral mastectomy; among women who have had preventive surgery, the risk of breast cancer is sufficiently low that they are not impacted adversely by the inability to breastfeed.

Other groups that have evaluated the relationship between breastfeeding and breast cancer risk among BRCA mutation carriers reported no relationship between breastfeeding and risk, although these studies were limited by small sample sizes and the merging of women who were carriers of a BRCA1 or BRCA2 mutation. These findings extend our previous report that breastfeeding for more than one year reduces risk among BRCA1, but not among BRCA2 mutation carriers.

In a collaborative re-analysis of data from 47 independent epidemiologic studies conducted among women in the general population, the authors reported a 4.3% reduction in breast cancer risk for every 12 months of breastfeeding (95% CI 2.9 to 5.8; P < 0.0001). The effect of breastfeeding among BRCA1 mutation carriers reported here is much greater than that reported in the general population (19% vs. 4.3% reduction in risk per year of breastfeeding). In BRCA mutation carriers specifically, it does not appear that parity per se influences the risk of breast cancer independently of breastfeeding. The majority of BRCA1-related tumors are basal-like breast cancers characterized by ER, PR and HER2 negativity while BRCA2-tumors resemble sporadic cases. Other groups have shown that parity is a risk factor, while breastfeeding protects against the development of basal-like or ER-negative/PR-negative breast cancers in the general population. Likewise, differences in the pathologic features of BRCA1 and BRCA2 tumors may also reflect etiologically distinct tumors and possibly differences in risk factor associations.

Several mechanisms have been proposed to explain the biologic basis for the inverse relationship between breastfeeding and breast cancer risk. These include: 1) hormonal changes, particularly a reduction in endogenous estrogen and progesterone levels and/or increased prolactin levels; 2) excretion of estrogens and carcinogens from the breast ducts; 3) breast tissue differentiation; and 4) a delay in the establishment of regular ovulation and, subsequently, the cumulative number of ovulatory cycles. We have recently shown that the number of lifetime ovulatory cycles does not influence breast cancer risk in women with BRCA1 or BRCA2 mutations (JK, JL, HTL, C K-S, SN, RD, WDF, PG, NT, PA, LS, Beth Karlan, AE, CE, Jeffrey Weitzel, DMG, JB, Dana Zakalik, CS, Taya Fallen, OG, TH, PS, SAN, Oophorectomy after Menopause and the Risk of Breast Cancer in BRCA1 and BRCA2 Mutation Carriers, submitted). Our data presented in this manuscript support the first three hypotheses and are reinforced by the long lasting effect of breastfeeding among BRCA1 mutation carriers. Breastfeeding for at least one year significantly reduced the risk of breast cancer diagnosed under the age of 50. Although the association did not achieve statistical significance (likely due to small numbers), this protective effect was also apparent for those diagnosed ≥ 50 and was indicative of a long-term reduction in risk with breastfeeding.

Experimental evidence supports an important role of the BRCA1 protein in mammary cell differentiation and proliferation. Rajan and colleagues have shown that BRCA1 and BRCA2 mRNA expression is high in proliferating cells in mice during periods of rapid proliferation and differentiation, such as embryogenesis, puberty and pregnancy, but is low during lactation. In addition, the BRCA proteins interact with STAT5a, a mammary gland transcription factor that is stimulated by prolactin at the end of pregnancy, and which is involved in the growth and terminal differentiation of breast epithelial cells. Thus, among women with a mutation and one functional allele, one would expect that breast cell differentiation from breastfeeding might be compromised.

In vivo studies have shown that a conditional mutation in Brca1 in mouse mammary epithelial cells results in defective development of mammary tissue during pregnancy and lactation. Further, Russo et al. have reported that the developmental pattern of breast tissue from parous women with a family history of breast cancer or BRCA1 mutation was comparable to that from nulliparous women with no family history (that is, did not differentiate with parity). Collectively, the evidence supports an important role of the BRCA proteins in breast tissue differentiation during pregnancy and/or lactation.

Based on our findings to date, it appears that cumulative sex hormone exposure, particularly estrogen, is likely involved in the development of breast cancer in BRCA1 mutation carriers. Late age at menarche, breastfeeding and bilateral salpingo-oophorectomy are protective; while the role of parity is less clear. Recent studies have identified an important role for progesterone in regulating the number of stem cells in normal human and mouse mammary glands. The terminal differentiation of mammary stem cells during the process of breastfeeding may be protective since this process can deplete the pool of potentially deleterious stem cells or by reducing the number of stem cells at risk of mutation. If confirmed, agents that can mimic the terminal differentiation process, or otherwise reduce the size of the stem cell population, may be effective in reducing breast cancer risk. Notably, it has been reported that heterozygosity of BRCA1 may result in abnormal self-renewal of breast cancer stem cells. Specifically, failure of terminal differentiation after pregnancy in BRCA1 mutation carriers resulted in an increased risk of breast cancer.

Strengths of the current study include the large number of known BRCA mutation carriers and the ability to conduct a matched analysis to ensure that the case and control subjects were similar. The sample size range in four prior studies was 94 to 1,601 BRCA carriers . To determine the effect of breastfeeding on cancer risk independent of the effects of parity, we limited our analysis to parous women and matched for parity. We controlled for other known or suspected risk factors for breast cancer in our multivariate models, thus decreasing the influence of confounding although our adjusted and unadjusted results did not differ substantially.

The main limitation of our study was the use of self-reported breastfeeding which may have led to measurement error; however, an earlier validation study by Kark et al. reported high concordance between breastfeeding derived from clinic records compared with an interview conducted 20 to 22 years later (Spearman P = 0.86). A role of recall bias is unlikely given that there is no reason for women to suspect a role of breastfeeding in the etiology of their disease. In addition, we were not able to differentiate between women who exclusively breastfed versus those who also supplemented with bottle feeding. Despite this, with 1,665 matched pairs, this is the largest study to date addressing the role of breastfeeding in the etiology of BRCA-associated breast cancer development.
Conclusions

In summary, these findings corroborate a protective role of breastfeeding on breast cancer risk for BRCA1. The lack of an association for BRCA2 mutation carriers suggests that the biological pathway for carcinogenesis is different for the two genes. Women with a BRCA mutation should be advised of the benefit of breastfeeding in terms of reducing breast cancer risk.

T.S. Wiley concludes, “This new study just reinforces these beliefs and gives us further information to aid BRCA1 carriers.”

Steven A Narod and TS Wiley



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LOW ESTROGEN? WHAT DOES THAT MEAN??

Hypoestrogen, What is that?
Women of all ages can have hypoestrogen. Hypoestrogen is when levels of cycling estrogen falls below the normal range of 150 pg/ml to 550 pg/ml. The symptoms are felt by women in many ways. And every woman knows when “the change” happens. Some women even know when slight changes begin to occur. Even the women who are lucky enough to never experience a hot flash often have probably experienced one of the following other hypoestrogen symptoms: heart palpitations, insomnia, mood swings, joint aches, headaches, fatigue, low libido, vaginal dryness, bloating, skin dryness, brain fog….just to name a few.

When just a few symptoms began to occur with me at age 42, I was NOT thinking it was from hypoestrogen. I knew that to be “menopause” and I was still cycling every 28 days having a 3-4 day period and just had two babies 15 months apart. When my doctor told me I should start on beta blockers to control my anxiety feelings and onset of heart palpitations, I decided to dig really deep and figure out what was causing the changes in my body to occur. I knew these changes came out of no where started to occur shortly after my last pregnancy at age 41. At that time my estrogen level was 48 pg/ml. I didn’t know much about fractionating the estradiol out of the estrogen total at that time. I didn’t know what the significance was about timing the cycling and checking blood. I didn’t know that fluctuations in estrogen can be pretty significant just days apart in a cycle. I also didn’t realize that if estrogen wasn’t peaking and I wasn’t ovulating I was not getting any progesterone and therefore had cycles with unopposed estrogen.

I’ve been treating women who have hypoestrogen levels and have seen the dramatic changes that occur when estrogen and progesterone are replaced in a cyclic dosing schedule and reach their individual therapeutic range in the blood serum. Like I said earlier, estrogen peaks around 350-550 pg/ml and is around 100-150 pg/ml on baseline days. Progesterone peaks around 10-15 ng/ml and is around 2-5 ng/ml on baseline days. Hormones that are too low cause symptoms that women feel and experience. They are real symptoms.

How long would you replace your thyroid if you were hypothyroid? I believe you would say forever. Well, I say that is how long we should replace our estrogen and progesterone if we have hypoestrogen. The results are amazing. It’s easier to replace hormones when receptors are still present and active. But, it is never too late. I have patients who are doing amazingly well that are in their late 70’s. I also have patients as young as 19 whose symptoms are resolved dramatically using bioidentical hormones in cyclic dosing and the results cannot even compare to that of traditional care, which is oral birth control pills (synthetic estrogen and synthetic progestins) given in static doses using low amounts of hormones. I know many women who cannot stand how they feel on the pill. Maybe some women don’t even realize that it is the pill causing some of the symptoms they experience.

Women can change the standard of care. My goal is to educate women and then we have a choice what we want to do with that information. We cycle. Let’s keep on cycling.


Hypoestrogen, What is that?

Lombard (630) 627-3700 to set up an appointment or email me at jones.gretchen@gmail.com

Did you hear about Pink Slime? Oh My!!

Gerald Zirnstein grinds his own hamburger these days. Why? Because this former United States Department of Agriculture scientist and, now, whistleblower, knows that 70 percent of the ground beef we buy at the supermarket contains something he calls “pink slime.”

“Pink slime” is beef trimmings. Once only used in dog food and cooking oil, the trimmings are now sprayed with ammonia so they are safe to eat and added to most ground beef as a cheaper filler.

It was Zirnstein who, in an USDA memo, first coined the term “pink slime” and is now coming forward to say he won’t buy it.

“It’s economic fraud,” he told ABC News. “It’s not fresh ground beef. … It’s a cheap substitute being added in.”

Zirnstein and his fellow USDA scientist, Carl Custer, both warned against using what the industry calls “lean finely textured beef,” widely known now as “pink slime,” but their government bosses overruled them.

If you have questions about “pink slime,” email us at ABC.WorldNews@abc.com.

According to Custer, the product is not really beef, but “a salvage product … fat that had been heated at a low temperature and the excess fat spun out.”

The “pink slime” is made by gathering waste trimmings, simmering them at low heat so the fat separates easily from the muscle, and spinning the trimmings using a centrifuge to complete the separation. Next, the mixture is sent through pipes where it is sprayed with ammonia gas to kill bacteria. The process is completed by packaging the meat into bricks. Then, it is frozen and shipped to grocery stores and meat packers, where it is added to most ground beef.

The “pink slime” does not have to appear on the label because, over objections of its own scientists, USDA officials with links to the beef industry labeled it meat.

“The under secretary said, ‘it’s pink, therefore it’s meat,’” Custer told ABC News.

ABC News has learned the woman who made the decision to OK the mix is a former undersecretary of agriculture, Joann Smith. It was a call that led to hundred of millions of dollars for Beef Products Inc., the makers of pink slime.

When Smith stepped down from the USDA in 1993, BPI’s principal major supplier appointed her to its board of directors, where she made at least $1.2 million over 17 years.

Smith did not return ABC News’ calls for comment and BPI said it had nothing to do with her appointment. The USDA said while her appointment was legal at the time, under current ethics rules Smith could not have immediately joined the board.

- Jim Avila, ABC News


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Joann Smith was formerly the president of NCA (NCBA) prior to her appointment to Undersecretary of Agriculture and then on to the board of IBP (USDA Inc.). She made Eldon Roth of BPI a very rich man. Roth was a major financing source for the USPB purchase of National Beef out of the Farmland bankruptcy. The recent sale of National Beef was highly profitable for the money men – cattle producers got sold out. – MC

Need More?
Advanced Meat Recovery – What is it?


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In Defense of Food

In Defense of Food
An Eater's Manifesto

Food. There’s plenty of it around, and we all love to eat it. So why should anyone need to defend it?

Because most of what we’re consuming today is not food, and how we’re consuming it — in the car, in front of the TV, and increasingly alone — is not really eating. Instead of food, we’re consuming “edible foodlike substances” — no longer the products of nature but of food science. Many of them come packaged with health claims that should be our first clue they are anything but healthy. In the so-called Western diet, food has been replaced by nutrients, and common sense by confusion. The result is what Michael Pollan calls the American paradox: The more we worry about nutrition, the less healthy we seem to become.

But if real food — the sort of food our great grandmothers would recognize as food — stands in need of defense, from whom does it need defending? From the food industry on one side and nutritional science on the other. Both stand to gain much from widespread confusion about what to eat, a question that for most of human history people have been able to answer without expert help. Yet the professionalization of eating has failed to make Americans healthier. Thirty years of official nutritional advice has only made us sicker and fatter while ruining countless numbers of meals.

Pollan proposes a new (and very old) answer to the question of what we should eat that comes down to seven simple but liberating words: Eat food. Not too much. Mostly plants. By urging us to once again eat food, he challenges the prevailing nutrient-by-nutrient approach — what he calls nutritionism — and proposes an alternative way of eating that is informed by the traditions and ecology of real, well-grown, unprocessed food. Our personal health, he argues, cannot be divorced from the health of the food chains of which we are part.

In Defense of Food shows us how, despite the daunting dietary landscape Americans confront in the modern supermarket, we can escape the Western diet and, by doing so, most of the chronic diseases that diet causes. We can relearn which foods are healthy, develop simple ways to moderate our appetites, and return eating to its proper context — out of the car and back to the table. Michael Pollan’s bracing and eloquent manifesto shows us how we can start making thoughtful food choices that will enrich our lives, enlarge our sense of what it means to be healthy, and bring pleasure back to eating.

Pollan’s last book, The Omnivore’s Dilemma, launched a national conversation about the American way of eating; now In Defense of Food shows us how to change it, one meal at a time.




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Reading Nutritional Labels on Foods We Eat

March 28, 2012

Do nutrition labels confuse you?

 
Nutritional labels have been around for well over a decade, and the familiar panel — which provides some key nutrition information, an ingredient list and nutrition declarations — enables more informed food decisions.
Do people make good use of the information? The first step is for people to bother looking at it -- and they do. Women more than men, health conscious and exercise enthusiasts more than couch potatoes, but most people report they do consult with the label, at least when they’re buying a product for the first time. A recent review of 120 studies of nutrition label usage in Public Health Nutrition finds that 75% of Americans check the label.

Eyeing the label is a good start, but do consumers get what they need from it?

A recent paper in Nutrition Reviews found that of the 60 percent of consumers who said they use the Nutrition Facts Panel, only a quarter found it easy to use. The calorie information on the Nutritional Facts Panel gets a glance from 75 percent of consumers, but most consumers cannot put the calorie count in context since they have no idea how many calories they should consume, and about half of the people overestimate their suggested daily caloric intake. The percent daily values, typically located above the actual ingredients, were either ignored or poorly understood by most surveyed.

A ‘D’ in label comprehension

A new study in the journal Appetite studied 120 young Israeli adults’ understanding of the various parts of the nutrition label. The study was performed in a travellers’ immunization clinic, so it’s by no means a representative sample of the population, but rather a group of highly schooled, mid to upper socio-economic class individuals.
People were presented with several common food products, and were asked about their attention to and understanding of the nutrition facts on the label.

Most of the people (almost 80 percent) reported that they looked at nutrition labels when selecting foods.
But when given a label comprehension evaluation, the average score was a ‘D’ – 60 percent correct answers.
The nutritional table was understood much better than the ingredient list or the nutrition declaration information.  The nutrition declaration piece, with its “without”, “contains no” and “less” assertions was least understood. When a bottle of canola oil declares it contains “no cholesterol” does it mean there’s naturally no cholesterol, or that this manufacturer kindly removed the cholesterol for added nutrition value?

Figuring out food labels

The nutritional label is an important tool for promoting healthy eating. Reading the label helps consumers decide if, and how much, of that packaged food they should eat.  Go to the site www.msgtruth.org to learn more about what the ingredients behind the labels actually means.

Some of the nutrition confusion can be solved by nutrition education – of which there currently is very little. Not all people know that ingredient lists, by law, have to list ingredients by their relative amount in the product, from high to low, so fruit as the first ingredient is very different from fruit at no. 5, and that added sugar comes has so many different names.   Recently, the Institute of Medicine advocated that the front of the package panel display only four nutrition facts: calories, saturated and trans fat, sodium and sugars. It recommends that the FDA develop a point system -- much like the energy star® program used for assessing electronics’ energy efficiency – which takes into account just saturated and trans fats, sodium, and added sugars, since these nutrients pose the most pressing diet-related health concerns.

To increase the mix-up, manufacturers introduce some more confusion in an effort to better market their product. The declaration “no cholesterol” on a vegetable oil is redundant – no vegetable oil has any cholesterol, as cholesterol is present only in animal derived foods. Likewise, package health claims promising “immunity” “antioxidants” "heart-health" “strong bones” and “lower cholesterol” don’t mean the food is healthy.  They practically don’t mean a thing.

So how to read the label? For an FDA tutorial on how to read the Nutrition Facts label go here, and I’d love to hear your personal approach.

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What Can We Do to Feel Better!

I am almost ready to publish my first podcast on Itunes and will post when it actually is ready to listen to. I am reading Suzanne Somers book BREAKTHROUGH and the table of contents outlines what she discusses and it's everything I have been talking about with my patients. She calls it 8 Steps To Wellness.

Step 1: Get Bioidentical Hormone Replacement Therapy
Step 2: Avoid Chemicals and Detoxify your Body
Step 3: Take Nutrition Seriously
Step 4: Create a Healthy GI Tract
Step 5: Avoid Pharmaceuticals Unless Absolutely Necessary
Step 6: Supplement Your Diet
Step 7: Exercise Regularly
Step 8: Get Proper Sleep

The goal here is to increase your life span as well as improve your overall health. Emphasizing early detection of illness, preventive strategies, and lifestyle changes.

Change is never easy. We get comfortable with our pharmaceutical drugs. Take a pill for every ailment we have.

These are the topics I will be discussing on my podcast shows. I hope you all will tune in and listen.


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Stay Tuned....

I am going to start doing podcasts and talk about hormones and treatment and symptoms. I'll keep you posted in the progress. I have lots to say about hormones and this web site is getting a little crowded and for some may be confusing to navigate through. If you would like me to send you weekly email updates letting you know when and how to hear these podcasts as they are scheduled, please send me an email letting me know at jones.gretchen@gmail.com.



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Estrogen and Cardiovascular Disease

Cardiovascular disease, which is the leading cause of premature death in the Western world, typically develops 10 years later in women than in men. Scientists have long established that the female hormone estrogen protects against the disease but the mechanism of action was unclear.

Professor Kinsella and Dr Elizebeth (Libby) Turner have shown that the prostacyclin receptor is a prime target for estrogen being regulated by the alpha (ERa), but not by the beta (ERb), form of the estrogen receptor protein. Prostacyclin receptor levels can prevent platelet aggregation, or blood clotting, and the narrowing of vessel walls. As such the protein can play a role in protecting the body from cardiovascular disease.

‘We found that prostacyclin receptor levels followed estrogen levels. If estrogen went down, so too did the amount of this prostacyclin receptor ', says Professor Kinsella. 'We now have a clear understanding of one of the ways that estrogen may protect against heart disease. This is really significant in its own right, as it opens up new avenues of investigation for treatment of cardio vascular disease in women and it adds considerable information to the whole debate about the potential benefits of hormone replacement therapy (HRT) for post-menopausal women.'

The Health Research Board funded this project. Commenting on today’s publication of the findings, Enda Connolly CEO of the state agency said, ‘Cardiovascular disease is the primary cause of death in Ireland. Approximately 10,000 Irish people die each year from this disease, so a finding like this, which sheds new light into the very core of the disease, has tremendous potential to create new and more effective treatments for patients.'

More information: Estrogen increases expression of the human prostacyclin receptor with the vasculature through an ERα-dependent mechanism. Elizebeth C. Turner and B. Therese Kinsella J. Mol. Biol. (2010) 396, 473-486.

Provided by University College Dublin



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What is the Truth about Menopause and Bioidentical Hormones? Read Here

I have been treating people with hormone problems for the past four years and the information that I have gathered is critical to your immediate and long term health and well being. Information your doctors don't have and the drug companies certainly don't want you to know.

Menopause is permanent! It is the Permanent Loss of your Sex Hormone System. Your ability to produce estradiol and progesterone depends on if you have any eggs left in your ovaries or if they are function-able! If you leave menopause untreated, it will affect your entire body. It causes numerous, immediate health problems, accelerates aging, and leads to the degenerative diseases of aging that women experience later in life.

I know estradiol and progesterone are essential to our health. They help us to be fit and functional today and over time, helps to prevent degenerative diseases like cancer, heart disease, type 2 diabetes, osteoporosis, blood clots, dementia, autoimmune diseases like arthritis and fibromyalgia. They also slow down the pace at which we age.

My patients who are absent of these two hormones are plagued by fatigue, abdominal weight gain, hair loss, constipation, headaches, digestive problems, brain fog and memory loss, irritability, anxiety, depression, loss of libido, vaginal dryness, insomnia, restless sleep, increased cholesterol, etc etc etc. The list is long ladies!

Some of you think you "skipped menopause" because you don't or didn't have any symptoms. Your body is still experiencing challenges you may be completely unaware of because no woman is escaping menopause. Menopause is permanent loss of your sex hormones. You never regain your ability to produce these two hormones. These hormones ARE essential to your health women!!

My approach to treating hormone loss is probably very different from what you have experienced from your doctor. Please understand, doctors are trained in medical school to treat ONLY THE SYMPTOMS of menopause. Not the cause!! The standard of care treatment is hormone drugs, patches, birth control pills, vaginal creams...Uggg

We can empower each other through education and knowledge. Fear and confusion has led women to believe that their own hormones are dangerous, cancer causing molecules! Oh my!! I really want this to change for women! My goal is to educate you and then you can make a choice. Similar to if you want to take supplements, vitamins, exercise, stop smoking, etc. You have that right to choose whether or not you do certain things that make you healthier. Shouldn't you have the same right to replace your hormones as well?

Read my article about proper levels of hormones in the body and learn what is optimal. Then, use only bioidentical transdermal hormones in cyclic, rhythmic dosing to acquire those levels. The results are self evident.




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How To Control Diabetes

In my medical training I was taught that we should eat a low fat diet high in complex carbohydrates and that prevented weight gain and disease. I have since discovered that I have been mislead down the wrong path. It isn't fat that makes us fat or have diabetes. In fact, it is the carbohydrates that we are eating. A diet high in fruit, milk, bread, and very little fat sets you up for higher blood sugar levels, high blood pressure, chronic fatigue, weight gain, and abnormal cholesterol profiles. Carbohydrates increase the release of insulin to bring blood sugar levels down. Insulin is a fat storing hormone. Weight gain, along with high insulin levels cause blood pressure to increase. The blood pressure medications often used often increase blood sugar levels even more.

You could test this yourself by monitoring your own blood sugar levels. Do an experiment of your own. Check your blood sugar levels when you get up in the morning before you eat and if you are not diabetic your blood sugar level should be "normal" which is between 70-100. Then eat a perfect American Diabetes Association breakfast, a bowl of shredded wheat with non fat milk, a banana and a glass of orange juice. Wow! Now watch your blood sugar rise one hundred to two hundred points. A normal blood sugar response to any meal is no more than ten to twenty points.

So it must be food that is the problem. It isn't protein. Protein will eventually turn into sugar, but not that quickly. It isn't the fat. We aren't eating any fats, or hardly any, and fats do not turn into sugar that quickly either. Carbohydrates are the only nutrient group that can be converted into sugar so fast. All carbohydrates are recognized as sugar by the body, whether they are in the form of grains, starches, dairy, fruits, or sweets. So basically we are telling diabetics to eat SUGAR!

Why is sugar so destructive to diabetics? To understand and appreciate why, you need to understand the role of insulin in the human body. Insulin is the hormone responsible for tightly regulating the amount of sugar going to the brain after you eat. Insulin accomplishes this in two ways. First, the presence of insulin alerts the liver to incoming high amounts of sugar so that the liver does not let this high sugar pass through to the brain. Second, insulin stows away sugar into cells, thereby decreasing blood sugar levels. Also, when sugar is stowed, insulin levels normalize. This system keeps blood sugars and insulin levels balanced.

Diabetics are insulin resistant. This means that cells will not allow insulin to unload sugar from the bloodstream. Because the cells do not respond to insulin, the pancreas reacts by secreting even more insulin in an attempt to open up the closed cells. The result is type 2 diabetics have both high insulin levels and high blood sugar levels. Now, ask a type 2 diabetic to eat more carbohydrates and it further increases both their blood sugar levels and insulin levels.

You can try this for yourself. Eliminate all obvious carbohydrate foods, such as potatoes, rice, legumes, cereals, breads, fruit, low fat yogurt, milk, and of course refined sugar. Add more eggs, egg substitutes, fish, chicken, red meat, nuts, non starchy vegetables, real mayonnaise, real cheese, real butter and healthy oils. See what happens. You will see that your blood sugar numbers will fall dramatically and you may even lose body fat.

Let's take this even further. Numerous studies reveal that diabetic patients have a very high rate of heart disease. These studies span three decades relating high insulin levels and heart disease, high insulin levels and hypertension, high insulin levels and excessive body fat gain and many other problems. What is interesting to me is that many people after a heart attack are told to go on a low fat, high carbohydrate diet. This increases their blood sugar levels which then increase the insulin levels. High insulin levels are associated with increase in weight, increase in blood pressure, degenerative diseases of aging such as osteoarthritis, various cancers, cholesterol abnormalities, coronary artery disease, less lean body mass with excess body fat, osteoporosis, stroke, and type 2 diabetes.

Could it be that we are accelerating the aging process through poor eating and lifestyle habits that raise insulin levels?

Of course there are genetic variables. However, this is clinically significant only when eating and lifestyle habits consistently cause insulin levels to rise. In other words, a genetic predisposition to disease is not a "guarantee" that you will develop that disease. Instead, what you do and how you live your life determines your risk for developing insulin resistance and the degenerative diseases of aging.

To learn more give me a call!


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The last show of 2011... Recap the 20 best HCG diet tips 12/28 by The hCG Diet Coach | Blog Talk Radio

The last show of 2011... Recap the 20 best HCG diet tips 12/28 by The hCG Diet Coach | Blog Talk Radio

Call my office Lombard (630) 627-3700 to set up an appointment or email me at jones.gretchen@gmail.com

What is the best delivery system for Bioidentical Hormones?

What’s the best delivery system for bioidenticals?

Generally, I try and put the hormones directly into the bloodstream without having to go through the stomach, intestine, and liver first. This is more physiologic (like normal human physiology) and does not cause adverse effects on clotting factors thus avoiding increasing one’s risk of stroke, heart attack, and venous blood clots.

There are five ways to do that:
1. Subdermal -- under the skin as with Pellets
2. Trans-dermal (through the skin as with patches, gels, or creams),
3. Vaginal suppositories or gel
4. Sublingual (under the tongue), or
5. Intramuscular injection (as with testosterone cypionate which is not quite bioidentical).

I prescribe compounded transdermal creams of female and male hormones quite frequently. With creams, it’s easy to change dosing and can be tailored just for you. It allows for more physiologic cycling if desired. However, it is more inconvenient and more costly, and the benefits might not exceed the costs for some people.

I use highly experienced compounding pharmacies who have excellent reputations amongst doctors like myself to make up these prescriptions for you.

Oral Prometrium or other progestin must be taken about 2 weeks a month or six days a week if you have your uterus still.

I hardly use sublinguals. They have to be dosed twice a day and allowed to dissolve under the tongue.

I’m using injectable hormones only for males, and it is called testosterone cypionate. I recommend injecting it once a week to reduce the peaks and valleys in blood levels.

I do not prescribe HGH (human growth hormone) in my practice at this time. It’s very expensive and its use is controversial.

For an excellent article on bioidentical hormones out of Harvard, go to http://www.health.harvard.edu/newsweek/What-are-bioidentical-hormones.htm



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Can't Sleep? Why Not?

The management of menopause today is a confusing and borders on negligence. As a result, women’s quality of life and longevity are being unnecessarily compromised. While health care professionals continue to debate about when menopause begins and ends, whether menopause should or should not be treated, and if so, with what, for how long, and by what delivery method, millions of women suffer needlessly and billions of health care dollars are pointlessly expended.

The current approach to managing menopause is either to do nothing or to simply treat its symptoms but not its cause. This approach is wrong, shortsighted, destructive and costly to women.

It is wrong for a number of reasons. One, this approach views menopause as merely a harmless transition out of a woman’s childbearing years during which she must cope with a number of temporary, bothersome symptoms, such as hot flashes, night sweats, mood changes, loss of libido, INSOMNIA, weight gain around our midsection, heart disease, bone loss leading to osteoporosis, forgetfulness leading to dementia.

Failure to treat menopause correctly is unacceptable to me! It is not as if menopause affects only a small fraction of the population. It affects all women who live to middle age — that’s 50% of the population, 100% of the time! Furthermore, the cause of menopause is absolutely known, as are its effects.

The medical profession is woefully misinformed about the long-term effects of menopause on a woman’s quality of life and well being. We didn’t used to live long enough for the ravages of menopause to be apparent!

In other words, we are in this mess due to misinformation, misunderstanding, and a lack of financial incentive to change it. Actually, if you ask me, for some, there is a tremendous disincentive to change it. The drug companies and hospital facilities make billions of dollars thanks to the mistreatment of menopause.

I practice what I preach. I treat menopause as the permanent loss of a hormone system. By treating the cause of menopause, I successfully help literally thousands of women slow down their aging process, defend against degenerative diseases, lose weight, have more energy, and generally feel better, while at the same time effectively treat such common menopause problems as:

• Hot flashes
• Sleep disruption
• Heart palpitations
• Night sweats
• Vaginal dryness
• Low sex drive and difficulty achieving orgasms.

By treating the cause of menopause, I have also been able to:

• Reduce cholesterol levels without cholesterol lowering medications
• Normalize blood pressure without blood pressure lowering medications
• Remedy sleep disorders without sleeping pills
• Improve blood sugar levels in women with diabetes without drugs or insulin
• Increase bone density without using anti-resorptive drugs.

The results are truly amazing!




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You Want to Feel Healthy Again, Lose Weight, Sleep Soundly...read on

What we do with our bodies begins when we are young and continues as we age. Healthy nutrition, managing stress, avoiding toxic chemicals, balancing hormones that are out of whack and exercise are all important to keep us healthy and age as slowly as possible. It is never too late to adopt better habits. To restore metabolism and achieve ideal body composition and obtain optimum health is a journey that will give you tremendous rewards. Let me guide you into this area of medicine that is not always discussed with Standard of Care physicians.

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Why Should We Worry About Menopause Symptoms?

We need to de-myth Menopause for both Women and Physicians. We are taught in medical school that menopause is no big deal and easy to treat. That's laughable. We are taught that our sex hormones are just for reproducing babies, fertility, and when we are done with our child bearing years why do we need them. We are taught that if we aren't having any symptoms we must be done with menopause. And yet, these women can't sleep, they have osteoporosis, they have mood problems, are on antidepressants, heart disease is around the corner, and so is memory loss. Menopause is PERMANENT and it means that estradiol and progesterone are gone. We are living longer and our system that makes our hormones is aging faster than we are dying. It is a degenerative aging of our reproductive system. We don't need to tough it out ladies. Another myth. Maybe because we were told that HRT is bad for us. That is due to the Women's Health Initiative Study on synthetic oral hormones; Premarin and Prempro. We are told HRT is not safe for us so just tough it out and here is your Zoloft or Prozac. What I believe is we need to treat the cause of menopause, not the symptoms. The cause is the loss of estradiol and progesterone in rhythmic cyclic levels.

We can do this together and I can teach you how to manage hormone replacement yourself with bioidentical hormone transdermal creams used in cyclic dosing. Without these hormones your body ages faster. Heart disease. Bone loss. Memory loss. Metabolism loss. Sleep disturbances. Just to name a few.

Let's educate ourselves women! Empower yourself with knowledge and spread the word.

Call my office in Lombard (630) 627-3700 to set up an appointment or email me at jones.gretchen@gmail.com