Have you read a good book lately? Most people sadly answer “No”. We all know the reasons for this; it is not worth it to enumerate the excuses, “But, by the neglect of the studies of the humanities, which has been far too general, the profession [and the public] loses a very precious commodity… There are at least a dozen or more works which would be helpful in getting wisdom in life which comes only to those who earnestly seek it.”1William Osler, the father of modern medicine said that.
I just got done reading “Bully Pulpit”, the history between Theodore Roosevelt and William Taft. Also, “Darwin’s Doubt”, which many scientists share today-the doubt, that is. In fiction I recently discovered the work of Jonathan Tropper: very funny and insightful on top of being a great writer, BUT, it is not for those who are easily offended when it comes to sex. And if you like philosophy, consider reading the book I am reading now, “Hegel and the Hermetic Tradition.” More on Hegel in my latest blog.
Reading has been shown to improve the care doctors provide. Patients’ health improves not only from better care, but, directly from their own reading.2
Hugo Rodier, MD
Mammogram controversy
In 2009 the US Preventive Task Force created a bit of a stir when they reported that women age 40-49 do not benefit from mammograms. It recommended starting mammograms at age 50. A lot of women and doctors were upset about that report and to this day continue to get and recommend mammograms at age 40. Well, the plot got “sicker”. A Canadian study reported last month that mammograms do not decrease mortality at all. The study also reported that 22% of positive mammograms are falsely positive, meaning there is no cancer despite the positive report.3Predictably, the study is getting blasted by “the establishment” as bad science. The main beef seems to be poor mammogram quality. Wherever the truth lies it cannot be seen clearly until we make sure money is not a factor in the discussion: funny, don’t you think?
Since mammograms are so entrenched in the system I anticipate that nothing will change for a while. In my practice I encourage patients to decide how and when to get screened. I also offer Thermograms. They do not radiate the breasts; they only pick up heat patterns from them.
In addition I discuss Xenoestrogens in the environment, the main reason we get any type of cancer. Remember that 85% of cancers are environmental,4a factor often underreported for political and economic issues.5We must limit exposure to environmental toxins like pesticides, plastics (BPA and phathalates), heavy metals, chlorinated products, hair permanents, rocket fuel and some chemicals in cosmetics and hygiene products. Phthalates just got more attention because they are found in many products we are exposed to: pesticides, time release medications, linoleum, vinyl (computers, cars), faux leather, shampoos and cosmetics-anything with fragrance).6
Keep you immune-detox system strong by maximizing gut health. By maintaining strong gut flora you lower the risk of cancer-see below. Good nutrition cuts down the risk of cancer by 2/3.7Overcoming a sugar addiction is the most important factor in improving our diet. Sugar increases the risk of cancer, a fact that won the Nobel Prize for Dr. Warburg in 1931. Below you will find excerpts from a landmark study reporting on specific foods that do that:
“Apoptosis by dietary factors.”8
- “In spite of substantial progress in the development of anticancer therapies, the incidence of cancer is still increasing worldwide. Recently, chemoprevention by the use of naturally occurring dietary substances is considered as a practical approach to reduce the ever-increasing incidence of cancer.”
- “By making modifications in the diet, more than 2/3 of human cancers could be prevented…. Dietary chemopreventive compounds offer great potential in the fight against cancer by inhibiting the carcinogenesis process through the regulation of cell defensive and cell death machineries.”
- “Apoptosis, a form of programmed cell death, plays a fundamental role in the maintenance of tissues and organ systems by providing a controlled cell deletion to balanced cell proliferation. The last decade has witnessed an exponential increase in the number of studies investigating how different components of the diet interact at the molecular and cellular level to determine the fate of a cell. It is now apparent that many dietary chemopreventive agents with promise for human consumption can also preferentially inhibit the growth of tumor cells by targeting one or more signaling intermediates leading to induction of apoptosis.”
- “The two major pathways that initiate apoptosis are extrinsic (death receptor-mediated,) and intrinsic (mitochondrial mediated.) Mitogenic and stress responsive pathways are involved in the regulation of apoptotic signaling. Noteworthy is the crosstalk between some of these pathways.”
Nutrients in… | Recommended Food |
ECGC | Green tea |
Curcumin | Turmeric |
Genistein | Soy |
I3C | Cruciferous |
Sulpharanes | Cruciferous |
Beta carotenes | Veggies |
Resveratrol | Grapes |
Isothiocyanates | Cruciferous |
Luteolin | Celery, green pepper, peppermint |
Lycopene | Tomatoes |
Anthocyanins | Pomegranate, wolfberry, plankton, algae |
Delphidin | Pigmented fruits, berries |
Lupeol, sylimarin | Mango, olive oil, herbs |
Gingerol | Ginger |
Capsaicin | Red pepper |
Sulfur | Onions, garlic |
“Emerging roles of the microbiome in cancer.”9
That is the title of a landmark article in the J. Carcinogenesis and a topic covered herein at nauseum. Read what the editors had to say about this:
“Gene-environment interactions underlie cancer susceptibility and progression. Yet, we still have limited knowledge of which environmental factors are important and how they function during tumorigenesis. In this respect, the microbial communities that inhabit our gastrointestinal tract and other body sites have been unappreciated until recently. However, our microbiota are environmental factors that we are exposed to continuously, and human microbiome studies have revealed significant differences in the relative abundance of certain microbes in cancer cases compared with controls. To characterize the function of microbiota in carcinogenesis, mouse models of cancer have been treated with antibiotics. They have also been maintained in a germfree state or have been colonized with specific bacteria in specialized (gnotobiotic) facilities. These studies demonstrate that microbiota can increase or decrease cancer susceptibility and progression by diverse mechanisms such as by modulating inflammation, influencing the genomic stability of host cells and producing metabolites that function as histone deacetylase inhibitors to epigenetically regulate host gene expression. One might consider microbiota as tractable environmental factors because they are highly quantifiable and relatively stable within an individual compared with our exposures to external agents.At the same time, however, diet can modulate the composition of microbial communities within our gut, and this supports the idea that probiotics and prebiotics can be effective chemoprevention strategies.The trajectory of where the current work is headed suggests that microbiota will continue to provide insight into the basic mechanisms of carcinogenesis and that microbiota will also become targets for therapeutic intervention.”
Unfortunately, most researchers are looking for a drug as a “therapeutic intervention.” How about the food we eat, as suggested by the editors?
1“My recent reading list of non medical books,” American J. Medicine 2014;127:101
2“Reading is fundamental,” J. Archives of Internal Medicine Med 2005;165:1943
3“Twenty five year follow-up for breast cancer incidence and mortality of the Canadian National Breast Screening Study: randomised screening trial,” British J, Medicine 2014;348:g366
4“Combating Environmental Causes of Cancer,” New England J. of Medicine 2011;364:7991
5“Environmental Factors are Underappreciated as Cancer Risks,” J. of the American Medical Association 2010;303:2456
6Epub J. Pediatrics Feb 3rd 2014
7J. Carcinogenesis 2007;28:233
8Ibid
9J. Carcinogenesis 2014;35:249