Cancer, Diet and Lifestyle: What We Know

Cancer, Diet and Lifestyle

Cancer develops by complex processes that are not yet fully understood. It is thought that the risk of development begins when the DNA is damaged possibly by reactive oxygen molecules, toxins, viruses and other reactive substances within cells. This is called the initiation phase. Most of the time, DNA is successfully repaired. When that does not occur, the next phase called promotion occurs where cells with damaged DNA divide into localized areas of the body. This process can occur from 10 to 30 years (“lag time.”). If there is still no repair, the next phase called progression can result with uncontrolled growth and spread of abnormal cells (metastasis) to other parts of the body (lung, liver, breast, bone, prostate, e.g.}.

According to Robert H, Lustig, MD, in his new book, Metabolical: The Lure and Lies of Processed Food, Nutrition, and Modern Medicine, epigenetics plays a strong role in gene expression. “Epigenetics refers to changes in the areas around our genes that can cause them to be turned on or off. Think of it this way: epigenetics is the on-off switch attached to the dimmer in your living room chandelier. The gene is the lightbulb, the epigene is the light switch. If the light bulb is defunct or the switch is frozen in the “off” position, the dimmer function is useless.” This may partly explain whether a disease or its risk is turned on or off. (SJF)

The eight leading environmental factors (other than genetic) related to cancer development are:

Obesity

Low vegetable and fruit intake

Physical inactivity

Smoking

Excess alcohol intake

Unsafe sex

Air pollution

Hepatitis B or C viral infection

DIET MODIFICATIONS

Consume a nutrient dense, whole-foods diet that predominantly includes plant foods. As Michael Pollan puts it, “Eat food, not too much, mostly plants.” Plant foods are rich in nutrients and phytochemicals that work synergistically to prevent many chronic diseases, primarily heart disease and cancer. Evidence exists that up to 45% of colon cancer cases could be avoided through diet and lifestyle changes alone.

Limit your consumption of high-calorie dense foods, primarily in the form of ultra-processed foods that are major contributors to weight gain leading to type 2 diabetes, or insulin resistance.

Cancers of the liver, pancreas, endometrium, colon, rectum, breast, and bladder are at higher risks for developing in obesity. Being overweight also raises the risk of developing non-Hodgkin’s lymphoma, multiple myeloma and gallbladder, liver, cervical, ovarian, and aggressive prostate cancers.

Be as lean as possible without becoming underweight. . The increased risk of disease appears to be due to a higher prevalence of metabolic disorders in many obese people. Approximately 70% of obese persons have two or more metabolic abnormalities such as:

Hypertension

Elevated triglycerides, glucose and/or insulin

Low HDL cholesterol (“good cholesterol”)

High C-reactive protein (a key marker of inflammation)

It may be helpful to be able to calculate your own weight status by using the Body Mass Index (BMI)You simply divide your weight in pounds by your height in inches squared X 703.

For example: BMI =140 pounds divided by 64 inches squared (4096) X 703 = 24.0. A healthy BMI is 20 – 24. Being underweight is considered a BMI of less than 19.0.

Limit your consumption of red meat (including beef, pork and lamb).  There are several reasons:

The International Agency for Research on Cancer (IARC) classifies red meat as a “probably carcinogen”.  You don’t need to give up meat; however, an intake of up to 18 ounces a week can be safely consumed without too much concern. BTW, 4 oz. is about the size of a deck of cards.

Another factor that raises cancer risk is the overcooking of red meat that produces charred areas of the meat – goodbye grill marks?). These create carcinogenic hetero cyclic amines (HCAs) that have been linked to pancreatic and colon cancers.

Another carcinogenic compound comes from burning the fat from meat when grilling that produce polycyclic aromatic hydrocarbons (PAHs), linked to stomach cancer.

Hint: Both compounds can be lessened by using a marinade on the meat.

Highly processed meats such as bacon, hot dogs, and lunch meats are known for their nitrite and nitrate content used as preservatives.  Smoking meats can lead to the formation of N-nitroso compounds which are considered carcinogenic.

Avoid deep-fried foods. When cooked in this manner, foods are exposed to a chemical called acrylamide that increases the risk of prostate cancer.

There are other lifestyle factors that can influence epigenetically the risk of any chronic disease. Alcohol intake, for example is important due to the carcinogenic effects of alcohol itself. 

“Chronic inflammation, which is strongly associated with being overweight, can increase the risk of developing cancer.  Excess belly fat produces hormones that can raise levels of insulin, estrogen and leptin, all of which have been linked to cancer development.” (Finlayson, 2019). 

The interconnected factors that trigger chronic diseases are vast and subject to manipulation by the body as well as our microbial environment. It would be wise to attempt to take the best care of your body as you possibly can and begin at an early age.  Aging as you know itself becomes a central factor in the development of any chronic disease. In 1980, Dr. James Fries, Professor of Medicine, Stanford University introduced the compression of morbidity theory. This theory states that “most illness was chronic and occurred in later life and postulated that the lifetime burden of illness could be reduced if the onset of chronic illness could be postponed and if this postponement could be greater than increases in life expectancy.”). That theory tells it all. (Unknown source). SJF

Source: Judith Finlayson. You Are What Your Grandparents Ate: What You Need to Know About Nutrition, Experience, Epigenetics & the Origins of Chronic Disease, 2019

Judith E. Brown, Nutrition Now, 7th Edition, 2013

Can Diet Affect Your Telomeres?

Glossary:

Apoptosis: the death of cells which occurs as a normal and controlled part of an organism’s growth or development. Also called programmed cell death.

Senescence: the state that cells reach when they stop dividing but do not die.

Telomeres: bits of DNA at the end of a chromosome that protects it during the process of cell division.

Telomerase: an enzyme, often referred to as “anti-aging” that maintains telomeres, helping to keep them long.

Telomeres shorten with age and progressive telomere shortening leads to senescence and/or apoptosis. Older people with shorter telomeres have three to eight times increased risk to die from heart disease and infectious diseases, respectively. Rate of telomere shortening is therefore critical to an individual’s health and pace of aging. Smoking, exposure to pollution, lack of physical activity, obesity, stress, and an unhealthy diet increase oxidative burden and rate of telomere shortening. To preserve telomeres and reduce cancer risk and pace of aging, we may consider to eat less; include antioxidants, fiber, soy protein, and healthy fats (derived from avocados, fish, and nuts) in our diet; and stay lean, active, healthy, and stress-free from regular exercise and meditation. 

Healthy foods such as tuna, salmon, herring, mackerel, halibut, anchovies, catfish, grouper, flounder flax seeds, chia seeds, sesame seeds, kiwi, black raspberries, lingonberries, green tea, broccoli, red grapes, tomatoes, olives area excellent choices. These combined with a Mediterranean type of diet containing whole grains would help protect telomeres.

Source: Telomeres, lifestyle, cancer, and aging

Current Opin Clin Nutr Metab Care. 2011 Janurary; 14(1):28-34

A study published in 2018 looked at fiber intake and telomere length in over 5,000 U.S. adults.

Researchers found there was a significant linear relationship between fiber consumption and telomere length. The more fiber subjects consumed, the longer their telomeres tended to be.

Here’s what the authors found:

“A difference of 4.8 to 6.0 years in cell aging was found between those in the lowest compared with the highest quartiles of fiber intake. Overall, the present study highlights the risk of accelerated aging among U.S. women and men who do not consume adequate amounts of dietary fiber.”

The study reported subjects were eating an average of 13.6 grams of fiber per day before starting the study, which is less than 50% of the Dietary Guidelines for Americans.

The Dietary Guidelines for Americans recommends the intake of 14 g of fiber per 1000 calories.

  • 2000 calories per day = 28 grams of fiber
  • 2500 calories per day = 35 grams of fiber

The best part is some of the most healthy and delicious foods pack the fiber.

It seems a few servings of high fiber foods per day keeps the telomere shortening at bay.

Source: Dietary Fiber and Telomere Length in 5674 U.S. Adults: An NHANES Study of Biological AgingDietary Fiber and Telomere Length in 5674 U.S. Adults: An NHANES Study of Biological Aging

Cancer, Diet and Lifestyle

Lifestyles can interact with the epigenome, defined as the network of compounds around our genes that are capable of altering gene expression in response to environmental influences. The ultimate action can result in cancer prevention.

DIET MODIFICATIONS

The general risk factors of cancer include obesity, physical inactivity, alcohol consumption and/or poor nutrition. These factors have the potential to determine if a cancer will result or in the opposite case, be suppressed.

Consume a nutrient dense, whole-foods diet that predominantly includes plant foods. As Michael Pollan puts it, “Eat food, not too much, mostly plants.” Plant foods are rich in nutrients and phytochemicals that work synergistically to prevent many chronic diseases, primarily heart disease and cancer. Evidence exists that up to 45% of colon cancer cases could be avoided through diet and lifestyle changes alone.

Limit your consumption of high-calorie foods, primarily in the form of ultra-processed foods that are major contributors to weight gain leading to type 2 diabetes, or insulin resistance.

Cancers of the liver, pancreas, endometrium, colon, rectum, breast, and bladder are at higher risks for developing in obesity. Being overweight also raises the risk of developing non-Hodgkin’s lymphoma, multiple myeloma and gallbladder, liver, cervical, ovarian, and aggressive prostate cancers.

Be as lean as possible without becoming underweight. It may be helpful to be able to calculate your own weight status by using the Body Mass Index (BMI).

You simply divide your weight in pounds by your height in inches squared X 703.

For example: BMI =140 pounds divided by 64 inches squared (4096) X 703 = 24.0. A healthy BMI is 20 – 24. Being underweight is considered a BMI of less than 19.0.

Limit your consumption of red meat (including beef, pork and lamb).  There are several reasons:

The International Agency for Research on Cancer (IARC) classifies red meat as a “probable carcinogen. You don’t need to give up meat; however, an intake of up to 18 ounces a week can be safely consumed without too much concern.” BTW, 4 oz. of meat is about the size of a deck of cards. (Finlayson, 2019)

Another factor that raises cancer risk is the overcooking of red meat that produces charred areas of the meat – goodbye grill marks?). These create carcinogenic heterocyclic amines (HCAs) that have been linked to pancreatic and colon cancers.

Another carcinogenic compound comes from burning the fat from meat when grilling that produce polycyclic aromatic hydrocarbons (PAHs), linked to stomach cancer.

Hint: Both compounds can be lessened by using a marinade on the meat.

Highly processed meats such as bacon, hot dogs, and lunch meats are known for their nitrite and nitrate content used as preservatives.  Smoking meats can lead to the formation of N-nitroso compounds which are considered carcinogenic.

Avoid deep-fried foods. When cooked in this manner, foods are exposed to a chemical called acrylamide that increases the risk of prostate cancer.

There are other lifestyle factors that can influence epigenetically the risk of any chronic disease. Alcohol intake, for example is important due to the carcinogenic effects of alcohol itself. 

“Chronic inflammation which is strongly associated with being overweight, can increase the risk of developing cancer.  Excess belly fat produces hormones that can raise levels of insulin, estrogen and leptin, all of which have been linked to cancer development.” (Finlayson, 2019). 

The interconnected factors that trigger chronic diseases are vast and subject to manipulation by the body as well as our microbial environment. It would be wise to attempt to take the best care of your body as you possibly can and begin at an early age.  Aging as you know itself becomes a central factor in the development of any chronic disease. In 1980, Dr. James Fries, Professor of Medicine, Stanford University introduced the compression of morbidity theory. This theory states that “most illness was chronic and occurred in later life and postulated that the lifetime burden of illness could be reduced if the onset of chronic illness could be postponed and if this postponement could be greater than increases in life expectancy.”). That theory tells it all. (Unknown source). SJF

Source: Judith Finlayson. You Are What Your Grandparents Ate: What You Need to Know About Nutrition, Experience, Epigenetics & the Origins of Chronic Disease, 2019

Working for an extension of a Healthy Lifespan

YOU ARE WHAT YOUR GRANDPARENTS ATE

The following post expresses the views of a blog titled Doctor’s Digest and not necessarily the views of Food, Facts and Fads. However, in the field of nutrition, there are always many controversies and it is wise to keep these in mind when seeking diet advice. The following article presents some concepts that are not yet proven by research; however, the future of epigenetics may provide more insight into these hypotheses. The source was based on the book, You Are What Your Grandparents Ate that was sent to me by the authors for review. See the Source below.

In other words:

Out on the edge you see all kinds of things you can’t see from the center. Big, undreamed-of things-the people on the edge see them first. Kurt Vonnegut

http://thedoctorsdigest.com/epigenetics-grandparents-ate

CLICK HERE.

Source:

You Are What Your Grandparents Ate: What You Need to Know About Nutrition, Experience, Epigenetics & the Origins of Chronic Disease. Judith Finlayson, 2019.

Foreword by Dr. Kent Thornburg, Professor of Medicine and Director of the Center For Developmental Health at the Knight Cardiovascular Institute, and Director of the Bob and Charlee Moore Institute for Nutrition and Wellness at Oregon Health and Science University in Portland, Oregon.

“This book explains why we are suffering the largest health epidemic in human history, why we need better wholesome foods to buy, why we need better food policy and why we must pay careful attention to the health and nutrition of our young women and men as they prepare to bear the next generation.”

You Are What Your Ancestors Ate


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Epigenetics and DNA

Why is what pregnant women eat before, during, and after pregnancy so important to the development of the unborn embryo/fetus? Recent evidence indicates that environmental factors may play an important role during early life development with potential long-term effects on health in later life. How do these factors influence the genes we already have in place?

There is an emerging concept called “early programming” that simply states that the fetus adapts to its existing environment when it is less than optimal, e.g., when the diet is lacking in essential nutrients for its development. This results in suboptimal development with long-term implications leading to increased risk of diseases such as heart disease, obesity, metabolic syndrome, glucose intolerance, or insulin resistance in adulthood. We now know that genes are switched on and off leading to functional physiological differences between individuals.

How are our genes modified? The most common alteration is a change in the nucleotide called single nucleotide (polymorphism (SNPs). For example, a SNP may replace the nucleotide C (cytosine) with the nucleotide T (thymine) in a certain position in a person’s DNA. This change is permanent.

Another way is through epigenetics. Epigenetics is the study of any change to our DNA that modulates a gene’s activity by turning them on and off. They result from exposure to the world – everything we eat, drink, breathe, feel and do, i.e., our environment. They are temporary so it is possible to correct our previous behaviors such as smoking cessation, exercising more or improving our diets to provide a more favorable health status.

The nutrients we extract from food enter metabolic pathways where they are formed into the molecules the body can use. One such pathway is responsible for making methyl groups. The methyl groups are epigenetic tags that attach to our DNA to modulate its activity to silence genes. Another epigenetic process is the production of acetyl groups (acetylation) to DNA histones that enhances the expression of the gene. So one pathway “turns off” the gene and the other “turns it on.” These modifications are particularly important during development of the fetus. Some modifications continue to have an effect into adulthood.

Nutrients like folic acid, B vitamins, and others are key nutrients in these processes. Diets of pregnant women high in these nutrients can rapidly alter gene expression, especially during early development when the epigenome is first being established.

What foods are rich in epigenetic nutrients? The list may sound familiar.

Leafy vegetables, seeds, nuts, liver, meats, whole grains, egg yolks, red wine, soy, broccoli and garlic provide methyl groups or are involved in acetylation. For example, sulphoraphane in broccoli increases acetylation turning on anti-cancer genes. Butyrate (a compound produced in the intestine when dietary fiber is fermented) turns on protective genes. Folic acid, vitamin B6  and vitamin B12 provide methyl groups.

Animal studies have shown that a diet with too little methyl-donating folate or choline before or just after birth causes certain regions of the genome to be under-methylated for life. This can produce permanent changes.

For adults too, a methyl-deficient diet leads to a decrease in DNA methylation, but the changes are reversible when methyl is added back to diet. So changes in the diet can create a healthier environment to help to prevent chronic diseases, but the behaviors need to change.

To fully illustrate the epigenetic process, one must tell the story of the agouti gene. All mammals have a gene called agouti. When a mouse’s agouti gene is completely unmethylated, its coat is yellow and has a high risk for obesity.  When the agouti gene is methylated (as it is in normal mice), the coat color is brown,  the mouse has a normal weight and less disease risk.   The mice are genetically identical but the fat yellow mice are different because they have an epigenetic “mutation.” in this case the presence or absence of methyl groups in its DNA.

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In a study pregnant yellow mice were  fed a  a methyl-rich diet;  most of her pups were brown and stayed healthy for life. These results show that the environment in the womb influences adult health.

The Emerging Field of Nutrigenomics

Possibly in the future of diet and nutrition there may come a time when we can use the concept of nutrigenomics to better understand why one person reacts to a particular dietary intervention more than another does. This may also explain why nutrition research is so erratic with studies reporting conflicting results and conclusions.  In the future, there is the potential for genetic testing that will result in genetic profiles that can aid in forming personalized diets and fitness plans, which will help minimize risks for disease.

We all know that a nutrient-rich diet is healthy and it is becoming increasingly clear that it  is not only what we eat in a lifetime but what our parents ate before our conception that can make a difference in our health status in adulthood.