May
01
2004

Chronic Inflammation Causes Cancer, Heart Attacks And More

When the Time Magazine devotes 7 full pages in the March 22, 2004 issue to the topic of inflammation as the source of most of the diseases of the Western World, you know that something important is happening in medicine. Christine Gorman and Alice Park have summarized some of the groundbreaking research of the past few years in this article. I will report about this article here, but also include direct links regarding some of the relevant research the authors have mentioned including some of the key links regarding the metabolic syndrome, which was not mentioned in the article.

Since the beginning of the obesity wave in North America it has become obvious that a cluster of diseases such as heart attacks, strokes, Alzheimer disease, cancer of the colon, multiple sclerosis, arthritis and others have also become more frequent. Dr. Paul Ridker, a cardiologist at Brigham and Women’s Hospital, was one of the pioneers of investigating inflammation as a possible cause and the common denominator of these diverse illnesses. He noticed that certain patients got heart attacks although their blood LDL cholesterol levels (the “bad” cholesterol) were normal. The theory at that time was that all patients who would develop heart attacks would come from a high-risk group of patients with elevated LDL cholesterol. The problem was that 50% of patients with heart attacks had normal LDL cholesterol levels. Dr. Ridker suspected that the C-reactive protein (CRP), which is found to be elevated in the blood of rheumatoid patients, would be somehow involved in the disease process of hardening of the arteries before a heart attack would occur. CRP is produced by the liver cells and by the lining cells of arteries in response to a general inflammatory reaction in the body. Examples of this would be rheumatoid arthritis patients and patients with autoimmune diseases, where CRP levels can be readily measured with a blood test. Dr. Ridker found that there was a very good correlation between the CRP level and the degree of inflammation as well as the risk for developing heart attacks and strokes. Further investigation by others confirmed that CRP levels were perhaps more important than LDL levels in predicting impending heart attacks. This is so, because CRP is the body’s substance in the blood stream that would be responsible for breaking up LDL containing deposits (plaques) in the walls of the arteries, which leads to heart attacks in the heart and to strokes in the brain.

Chronic Inflammation Causes Cancer, Heart Attacks And More

Chronic Inflammation Causes Cancer, Heart Attacks And More

Other investigators found that CRP was only one link in a complex chain of events that includes inflammatory substances (cytokines) from the fat cells as well as insulin and insulin-like growth factors from the metabolic syndrome. Leptins are also a factor as has been discussed under this link.
Dr. Steve Shoelsen from the Joslin Diabetes Center in Boston has developed a mouse model for the metabolic syndrome. These mice will produce huge amounts of inflammatory substances in their fatty tissue in response to any inflammatory process that is started in them. Anti-inflammatory drugs such as the statins or metformin, it is hoped, will be shown conclusively to dampen the inflammatory process and prevent heart attacks, strokes and diabetes as well as cancer, Alzheimers disease and arthritis. Heart disease has already been shown to be improved by anti-inflammatory drugs. Asthma is an inflammatory disease of the small bronchial tubes, which can be stabilized with the anti-inflammatory drug Avastin.

What can we do as consumers to prevent some of those life-threatening diseases? By reducing our weight through calorie restriction on a low-glycemic diet we can help to reduce the insulin-like hormone substances of the fatty tissue. Regular exercise of at least 30 minutes of a brisk walk daily or the equivalent of other sports activities will half our risk for colon cancer and many other cancers. A diet rich in fruits and vegetables as well as fish and fish oils will reduce the amount of free radicals in our system cutting down on the circulating inflammatory substances. This prolongs life, prevents all of the major diseases of modern civilization and leads to longevity as the study of the Okinawa diet has shown.

Based on an article in the Time Magazine, March 22, 2004 edition, page 54 to 60.

Here is a chapter on arteriosclerosis from the Net Health Book, which explains inflammatory changes of the arterial wall:

http://nethealthbook.com/cardiovascular-disease/heart-disease/atherosclerosis-the-missing-link-between-strokes-and-heart-attacks/

Last edited October 26, 2014

May
01
2004

Sugar And Starchy Foods Cause Colorectal Cancer

A study from the Harvard University involving 38,000 women and having been started in 1993 has surprised the researchers. They wanted to find out whether there were certain foods that may cause colon and rectal cancer. So they administered a “food-frequency” questionnaire with 131 questions to women 45 years or older who entered into the study. Such factors as low-dose aspirin, vitamin E and beta-carotene were included in the questionnaire as was the exact food composition for the year prior to enrolment into the study.

A sugar load (glycemic load) was calculated. This way the impact of various sugar and starch containing foods could be assessed and compared among different subgroups regarding the later development of cancer in the colon and rectum.
When Dr. Susan Higginbotham and Dr. Simin Liu analyzed the diets of the 174 patients who did develop cancer (26 rectal cancers, 148 colon cancers) they found that the women with the highest sugar and starch load were 3 times more likely to develop cancer than the controls with a low glycemic load. High glycemic load foods are candy, cakes, cookies; any other refined flour products including white bread, pasta, French fries and baked potatoes. Together with other literature in this field the authors of this study concluded that the high glycemic food load leads to increased insulin levels in the blood as well as insulin-like growth factors. This in turn leads to cell division in normal and cancerous cells including the lining of the colon and rectum. In addition it is known that the C-reactive protein promotes an inflammatory response that will lead to heart attacks and to cancer.

Sugar And Starchy Foods Cause Colorectal Cancer

Sugar And Starchy Foods Cause Colorectal Cancer

Dr. Bob Bruce from the University of Toronto has shown in his research on colon cancer that insulin and related factors are important in the promotion of this cancer. He commented regarding the Harvard study reviewed here that more research is required before the exact cause of cancer of the colon and rectum would be understood. This knowledge is required before more effective preventative measures can be found other than a simple reduction of sugar and starch in the foods we eat.

Based on the Feb.4 edition of the Journal of the National Cancer Institute (U.S.) and the National Review of Medicine (Canada) March 15, 2004.

More info about Colorectal cancer can be found through this link.

Last edited October 26, 2014

Apr
01
2004

Breast Cancer And Miscarriages; Fear-Mongering Debunked

For many years there were conflicting reports about the emotionally charged topic of whether miscarriages (=spontaneous abortions) or induced abortions (also simply known as abortions) would lead to an increased risk for these women later in life. The problem was that the studies could not be directly compared because they differed in size, in age group and whether the women had one or more children or none.

The studies also differed in respect to whether they were prospective or restrospective. In this context a prospective study is one where it was known at the outset before the women developed breast cancer whether or not there was a history of a spontaneous or induced abortion in the past. A retrospective study would be one where a group of women with established breast cancer would be asked retrospectively whether or not they had a history of abortions (spontaneous or induced).

It turns out that the discrepancies between these studies in the past were largely because of the significant difference between the data of the unreliable retrospective studies and the very reliable prospective studies.

On March 27, 2004 the Lancet reported about a study that had been undertaken by the Collaborative Group on Hormonal Factors in Breast Cancer (seat of the Secretariat in Oxford, England). This study involved hundreds of scientists and clinicians from the major Cancer Clinics around the world who gathered the world-wide epidemiological evidence about breast cancer and pooled the data regarding 53 studies from 16 countries.

Breast Cancer And Miscarriages; Fear-Mongering Debunked

Breast Cancer And Miscarriages; Fear-Mongering Debunked

A total of 83,000 women with breast cancer around the world had been included in this study. The data was separated into sub-categories. For instance, 44,000 women were included in the prospective branch of the study and 33,000 in the retrospective branch. The data was carefully controlled for the factors mentioned above and many other differences to ensure that the data could be compared (rules of evidence-based medicine).

The surprise finding was that there was no statistical difference regarding the risk for developing breast cancer in the prospective branch of the study between the group of women who never were pregnant, those who had one or more children and those who had miscarriages or abortions in the past. However, the retrospective studies reported a higher incidence of breast cancer because of an observer bias. The researchers and clinicians concluded that the data of the restrospective studies were unreliable because they were not carefully controlled and there likely was more reliable reporting of the women who had developed breast cancer than the control groups who likely underreported their histories thus resulting in misleading conclusions.

Summary: Women do not have a higher risk of developing breast cancer following spontaneous or induced abortions. Forget all of the fear-mongering that you may have heard in the past in the popular press.

More information about causes of breast  cancer: http://nethealthbook.com/cancer-overview/breast-cancer/causes-breast-cancer/

Lancet 2004; 363: 1007-16.

Last edited October 26, 2014

Apr
01
2004

Lycopene Of Tomatoes Fights Cancer Cells

Dr. John Erdman Jr. from the University of Illinois has done epidemiological studies that suggest that the red color of tomatoes, which is provided by lycopenes, is only effective against prostate cancer, if the whole tomato is consumed.

The professor of food science and human nutrition found that other phytochemicals in the tomato act in concert with lycopene to protect against cancer. To prove this more conclusively, he designed an experiment involving 194 rats with prostate cancer into three groups.

Group 1 was the control group without any detectable lycopene in their diet. Group 2 was fed the control diet with purified lycopene. Group 3 was fed the control diet with ground-up tomato paste (with seeds and skins). Group 3 was the only group where the risk of dying from prostate cancer was reduced by 30%. Group 2 rats had the same high death rates as the control group. These results were recently published in the Journal of the National Cancer Institute.

Dr. Erdman concluded that taking lycopene is not as effective as eating the whole tomato to prevent cancer of the prostate. He also suggested to use whole tomato products in tomato juice, in salads, pasta and pizzas.

Lycopene Of Tomatoes Fights Cancer Cells

Lycopene Of Tomatoes Fights Cancer Cells

Based on an article in the Medical Post, Vol 40, No.8, Feb.24, 2004 (page 33).

Link to prostate cancer chapter of the Net Health Book.

Last edited December 8, 2012

Apr
01
2004

Less Death Rates From Breast Cancer With Exercise

At the 95th annual meeting of the American Association for Cancer Research in Orlando / Fla. the results of a study regarding the effect of exercise on breast cancer survival rates was presented. Dr. Michelle D. Holmes and co-workers (Harvard University in Boston) reported about data from the Nurses’ Health Study. About 2000 patients with breast cancer were identified in the period of 1984 to 1996 who were followed until the end of 2002. At that time 209 had died from their breast cancer. The investigators were able to control the data for all the other factors such as smoking, obesity, and many other factors except for the amount of exercise per week that these women were doing. The highest risk group was the one that did not exercise and the death rate of this group was set as 100% as can be seen in this table, which I constructed based on the published data.

The various groups as indicated on the bottom of the table were the hours exercised per week from 0 hours to more than 15 hours per week (this was expressed as metabolic equivalent of a brisk walk). It can be seen that survival from breast cancer can be influenced by as little as 3 to 9 hours of a brisk walk per week (about 20% reduction in death rate) and reaches a plateau at 9 to 15 hours of exercise per week (around 50% reduction in death rate).

Less Death Rates From Breast Cancer With Exercise

Less Death Rates From Breast Cancer With Exercise

The authors of the study said that when the data was expressed as recurrence of breast cancer, the same results were obtained. This study would indicate that even 30 minutes of exercise per day will reduce mortality in a patient with breast cancer. Also, it is known from other studies that exercise will be more effective in terms of cancer prevention in general including prevention of breast cancer.

Percentage of breast cancer death rates decreases with exercise (hours of exercise per week depicted)

Less Death Rates From Breast Cancer With Exercise1

Breast Cancer Death Rate Decreases With Exercise

 

Link to breast cancer chapter of the Net Health Book.

Link to Fitness: http://nethealthbook.com/health-nutrition-and-fitness/fitness/

Last edited October 26, 2014

Mar
01
2004

Genetic Manipulation For Terminal Cancer

Two publications recently highlighted the importance of the p53 gene that is located on the human chromosome 17, which has been dubbed the “guardian of the genome”.

It appears that its role is to suppress any cell that has damage of the genetic material (of the DNA). If the suppressor gene p53 is not working in a cell, it will continue to divide and become a cancer cell. Only, if the p53 gene is working properly, will the cell go through its normal life cycle, which includes cell birth, a certain period of life and cell death (“apoptosis”).

This sounds all very theoretical, but I will demonstrate with two examples from the current medical literature how this knowledge has already been used and will likely be developed further in a practical sense in cancer patients. The first paper has to do with repairing damaged p53 genes directly with genetic modifications. The second paper approaches this problem from a different angle. It deals with the other half of cancers that originate not from genetic defects of the p53 gene, but from an overproduction of inhibitors that are produced in the cell itself, particularly in many cancer cells. A new class of very promising compounds have been developed that can neutralize the action of the inhibitors and normalize p53 function.

1. The cancer treatment specialists at the M.D. Anderson Cancer Center in Houston/Texas have done several clinical trials where they have proven that with the help of gene transfers into tumor cells of lung cancer patients the survival in these previously hopeless cancer patients can be significantly improved. A summary of these studies has been published in the February 2004 edition of the Hematology/Oncology Clinics of North America.

Genetic Manipulation For Terminal Cancer

Genetic Manipulation For Terminal Cancer

45% to 75% of these types of lung cancers have the p53 gene deficiency and for this reason are particularly difficult to treat as they are not responsive to chemotherapy or radiotherapy. These researchers and many other researchers in this field have shown that the specialist can transfer the missing p53 gene back into the cancer cells in a number of ways and this way change their growth pattern. These modified cancer cells either stop behaving like cancer and the patient is cured (a certain percentage, but not the majority). On the other hand the changed cancer cells can often be rendered more sensitive to chemotherapy and radiotherapy, which happens in about 60 to 70% of the genetically treated cases. Overall it is now possible with a combination of gene therapy and chemotherapy and/or radiotherapy to get about a 50% response rate and about 20% cures on the longterm. In the past all of these patients would have died within a few months from the initial diagnosis. The researchers of that publication stressed that these new treatment approaches are not yet routine in cancer treatment, but that with further refinements there will soon be more hope for these difficult cancer patients. This would be applicable not only for the difficult to treat lung cancer patients, but also for many other types of soft tissue cancers that often have p53 gene deficiencies and that up to now have often been untreateable.

2. The second paper that fits into this topic was published recently in the January 2, 2004 issue of the magazine Science. Researchers from the Hoffmann-La Roche labs in Nutley, New Yersey, have found that a new class of smaller molecules is able to inhibit the main group of oncoproteins known as MDM2 inhibitors that interfere with normal p53 function. The molecular oncologists at Hoffmann-La Roche under chief researcher Lyubomir Vassilev have successfully undertaken research in this complex interaction between the life saving p53 gene action and the undermining effects of various oncogene proteins and in particular the MDM2 inhibitors. There are two such substances of a new class of potential drugs that seem to be particularly promising. The new class of drugs was coined “Nutlins” in honor of the site of where they were discovered. Nutlin-1 has been tested in cultured tumor cells and was able to boost p53 activity resulting in sudden normal function. The cancer cells stopped dividing and disintegrated (due to the normal tumor fighting action of the p53 gene).

Another similar molecule, called Nutlin-3, was fed to nude mice who are deficient in their immune system and that are used by cancer researchers as a model to grow various types of tumors. In this model there was a 90% cure rate, which is unheard of as usually 100% of these nude mice would die from any transplanted tumor. There were no demonstrable side-effects in these mice that survived. Drs. Vassilev and David Heimbrook from the Hoffmann-La Roche cancer drug unit pointed out that this type of effect is much better than any cancer drugs that are presently used, however they added that it will be very difficult to predict how quickly this could be translated into the human situation with clinical trials. There is definitely a niche for treating sarcoma, which is one of the more difficult to treat cancers. Other cancers would be malignant tumors of the connective tissues, of nerves, bones, blood vessels, fat, muscles, deep skin tissues and cartilage. Many of these as well as some lung cancers produce high levels of the MDM2 protein. It is these types of tumors that would be the most likely candidates for early human trials with the Nutlins.

References: 1. February 2004 edition of the Hematology/Oncology Clinics of North America (Volume 18 • Number 1 • February 2004), published by Saunders, and entitled “Gene replacement therapy for non–small cell lung cancer: a review”. 2. January 2, 2004 issue of the magazine Science.

Comment On Oct. 26, 2014: As can be seen from this reference in 2011 nutlins persist, but likely have to be combined with other specific anti-cancer agents in the future.

Last edited October 26, 2014

Jan
03
2004

China Blows Alarm Whistle On Smoking

The risks of smoking are being addressed in China, where roughly 300 million people or one quarter of the population are puffing away. The number is rising by about 3 million new smokers each year, and according to statistics of the WHO 700,000 die each year from smoking.

In November of 2003 China joined the Framework Convention on Tobacco Control (FCTC), a subsidiary of the World Health Organization. As a member China is now obliged to tighten restrictions on cigarette marketing and consumption.
Due to an economic boom in the country foreign tobacco giants are putting their hope into this rising market, as revenue has decreased elsewhere in the world. So far tobacco taxes, which are collected from the 1.7 trillion cigarettes sold in China amount to 8 billion $US or one tenth of government revenue. In the wake of SARS, however, the realization has come to the forefront, that health care cost have a severe impact on the economy of a country. Despite the seemingly enticing short-term gain from tobacco tax revenue, short cuts in health care can economically damage a country in the long run.

Health officials will have a battle with their counterparts in finance, when it comes to implementing tobacco control. In some areas of the country the sale of tobacco products to children has been banned and an attempt has been made to restrict cigarette commercials.

China Blows Alarm Whistle On Smoking

Quit smoking!

Powerful tobacco lobby groups actively undermine these efforts.
It is encouraging to see at least a beginning of public education about the risks of smoking. However, in a nation where cigarette manufacturing and consumption are the highest worldwide, it will be a long and arduous journey to clear the air to better health.

Based on The Lancet 363, No. 9402 (Jan. 3, 2004)

Last edited December 8, 2012

Dec
01
2003

New Tumor Marker For Prostate Cancer Detected

According to an upcoming article in the December 15th issue of Cancer (Cancer 2003;98) a research group from the Harvard Medical School, Boston, under Dr. Brian Liu describes a micro-dissection method where prostatic tissue from 17 suspected cancer patients were examined with a spectroscopic method for a new protein marker, the cellular protein PCa-24). This was found to be positive in 16 of the 17 samples. In contrast, 12 patients with benign prostatic hyperplasia (also known as BPH or “benign prostatic hypertrophy”) showed no trace of this prostate cancer specific protein. As this protein is located inside the prostate cancer cell (it is a cellular protein), one has to obtain a tissue sample through a prostate biopsy. The group under Dr. Liu achieved this through laser capture micro-dissection  Proteomics, which is the method that was used to characterize the prostate cancer specific protein (PCa-24), is briefly discussed under this link, but it is not necessary to understand all of the ramifications of these methods. What is important regarding the work by the group under Dr. Liu is to note that there is now a very reliable method available to distinguish between the harmless BPH condition and the deadly prostate cancer condition, which requires invasive therapy such as a radical prostatectomy. Both of these conditions can produce high prostate specific antigen (PSA) that can be detected in the blood. Dr. Liu’s group plans to develop antibodies to the PCa-24 protein so that eventually there will be a more specific blood test available that could be used in patients with high PSA levels to distinguish between benign and cancerous prostate conditions. In the future the physician might use the cheaper PSA screening test to screen for prostate abnormalities and use the more expensive antibody test against the PCa-24 protein that is being developed to determine whether or not prostate cancer might be the underlying cause.

New Tumor Marker For Prostate Cancer Detected

New Tumor Marker For Prostate Cancer Detected

Dr. Liu also wants to develop a high resolution body scan where in the case of metastatic prostate cancer the cancer cells would be located exactly where they are with a new imaging technique. These would have a high probability of being specific for prostate cancer, as the antibodies would be highly specific against the prostate cancer protein. Here is a link to the Net Health Book’s chapter on prostate cancer.

Last edited December 9, 2012

Aug
01
2003

HRT; Findings From The British Million Women Study

 

In the latest issue of the Lancet (Lancet 2003;362:414-415,419-427) a study from Great Britain was published regarding the risk of breast cancer. Over 1 million women were followed from 1996 to 2001. They were in the age group of 50 to 64. Of these 80% were postmenopausal, and these formed the basis of the study. Dr. Valerie Beral (from the Cancer Research group UK in Oxford) was the lead investigator. About half of the women were on various forms of hormone replacement therapy (HRT), the others were not and served as a control. Risks were always expressed in comparison to the controls without any hormone replacements. Here is a tabular summary of the various hormone replacement therapies and their risks of leading to breast cancer.

The relative risk of developing breast cancer did not significantly change whether HRT was taken orally, transdermally or through implanted formulations. Tibolone is a synthetic steroid used for postmenopausal symptoms and treatment of endometriosis.

Dr. Beral’s group has estimated that in Great Britain in the past 10 years about 20,000 additional cases of breast cancer were caused by HRT for menopause among women aged 50 to 64. Out of these about 75% were due to the use of the combination of estrogen/progestin.

HRT; Findings From The British Million Women Study

HRT; Findings From The British Million Women Study

An accompanying editorial by Dr. Chris van Weel stated that “general practitioners should discourage HRT for their patients” and, if used, should last “no longer than 3-6 months”. The investigators of this study suggested that “discontinuing HRT should be suggested in as supportive a way as possible, because no one will benefit from panic or over-reaction”.

Findings from the British Million Women Study on HRT
Detail of hormone replacement: Breast cancer risk compared to control:
overall risk of HRT for all groups of HRT 1.66-fold
women who stopped HRT the previous year 1.14-fold
estrogen only use currently 1.30-fold
estrogen-progestagen combination
1.88-fold
tibolone users
1.45-fold
combination HRT user less than 5 years 1.7-fold
combination HRT user more than 5 years 2.21-fold
equine estrogen combined with medroxyprogesterone acetate and taken at least 5 years 2.42-fold
death rates from breast cancer associated with current use of HRT 1.22-fold

Discussion: Please keep in mind that the British authors of this study were using the drug manufactured synthetic hormone-like substances and NOT bio-identical hormones. The outcome with bio-identical hormones would have shown the opposite, namely that women would not have developed heart attacks, strokes or cancer and they would not have died prematurely. Read more about bio-identical hormone replacement in the links below.

Here is a link to a chapter on menopause from Dr. Schilling’s Net Health Book.

This link deals with bioidentical hormone replacement (see lower half of that page).

Last edited October 26, 2014

Jun
01
2003

Exercise Saves Lives In Women Over 65

A recent study released in the Journal of the American Medical Association (JAMA Vol. 289 No. 18, May 14, 2003) has found a profound effect of exercise on the survivial of elderly women. Dr. Gregg et al. have followed 9518 women aged 65 or older for a total of 12.5 years with a follow-up visit in between at about the 6 year point. They found that women who exercised (walking, aerobics etc.) and who were compared with a control group who was sedentary (no form of exercise), had the following improved survival rates.

These findings were independent of other factors up to an age of 75 years. In other words, age, smoking, weight and a number of pre-existing diseases did not influence these improved survival figures from the effect of exercise. However, when a woman had a significant chronic disease or was older than 75 years of age, the survival improval from exercise was not as strong as indicated in the table above. Also, the follow-up visits showed that those women who exercised continually, had the highest survival advantage.

Exercise Saves Lives In Women Over 65

Exercise Saves Lives In Women Over 65

The bottom line: increasing and maintaining a physical exercise program will likely lead to a longer life. At the same time the exercise program needs to be started early enough to be of benefit to those who are older than 75 years of age.

Disease and death rate reduction from exercise in women aged 65 and over
Reduction of:
Effect of risk reduction:
overall death rates 48%
cardiovascular disease 36%
cancer 51%

Some of the Associations that were contributing to this important study were: The National Center for Chronic Disease Prevention and Health Promotion (Atlanta, Ga), the Graduate School of Public Health, University of Pittsburgh (Pittsburgh, Pa), the Prevention Sciences Group, Departments of Medicine and Epidemiology and Biostatistics, University of California (San Francisco) and the University of Minnesota and Section of General Internal Medicine, Veterans Affairs Medical Center, Minneapolis.

Here is a fitness link: http://www.nethealthbook.com/articles/fitness.php

Last edited December 9, 2012