As we push deeper into the year, I am getting closer to having to get back up in front of audiences for my main work. Provided I’m not spending all of my time presenting and can get a good balance, I generally don’t mind being up in front of audiences. Obviously presenting the paleo framework can have its challenges though. Convincing people they need more sleep and sunlight – generally an easy sell. Encouraging people they need to focus on low intensity exercise, get strong, and do some sprinting every now and then… a slightly harder sell, but I’m pretty confident I have got the formula right (especially as people see that they don’t have to live in the gym to achieve their fitness goals). But by far and away, presenting paleo nutrition can be a tough ask. Many, women in particular, struggle coming to terms with the prospect that the various health agencies that they have trusted are perhaps more concerned with looking after the economy or might be unduly influenced by vegetarians in high places. Some can get quite emotional regarding the prospect that bread is doing them harm, that they might need to give it up, that the diet regime that they have fruitlessly invested time in (and which has let them down time and again) was never going to work… I am lucky if I get 45-60 minutes to make my case for paleo nutrition. It’s a tough sell, unless you have some paleo-champions in the room who can back me up with their experiences (which I have had in a few places now).
The fact that I often need to call on the testimonial of someone to sway people highlights an issue in itself. I am well qualified for what I do… more so than many in this industry. I present extensively on the research and people can see how well referenced the information is. But I still often get treated like I have just all made it up unless I have someone there to say they went to their doctor and their doctor told them to go on the paleo diet. And this year, I seem to be going into all of this a bit jaded for that fight. I look at some of the other information that is getting put out into the public arena… what is published in the popular papers… the numerous dolly-bird dietitians-for-hire on TV at present selling fruit juice, breakfast cereals, etc, and I ask why the hell do I have to have 10 references for every single sentence I say, yet all of these other morons can say what they like and have it broadly accepted?
I had a bit of an example of this this morning when an item on the breakfast television programme here discussed a new report due out in the UK regarding a public advisory to eat less red meat due to it being associated with (reported as causing) an increased risk of bowel cancer. Brace myself for the inevitable ‘did you see ‘Breakfast’ this morning on red meat’ (often with a hint of ‘you recommend people eat lots of meat and meat gives you cancer so explain your way out of that one’.) The link to the video is here for those who want to watch annoying Petra interview a lame Beef & Lamb CEO who seems to just accept the science for how it has been reported… Not a reference in sight from either of them. Nor was there much in The Telegraph report on this subject…
Britons will be warned that they must cut their consumption of red meat to reduce the risk of cancer, following official advice from the Government scientists.
Consumers will be told to eat no more than 500g of red or processed meat each week, or 70g a day, under recommendations to be issued by the Coalition this week. The daily total is the equivalent of three rashers of bacon – while the weekly amount would be reached by eating one large steak, a pork chop, two sausages and a small portion of beef bolognese sauce.
A Coalition source said: “It is important that people are not put off eating red meat entirely – but it would be irresponsible to ignore the potential health risks. The advice is very clear.”
The recommendations will follow the publication of a full report by the Scientific Advisory Committee on Nutrition, which is due within days. The findings are expected to echo the committee’s draft report, which found that lower consumption of both red and processed meat would probably reduce the risk of bowel cancer, the second most common cause of cancer death in Britain.
The experts will say the full study has confirmed the link between higher meat consumption and cancer, but is not able to quantify this fully, partly because of the complexity of the data examined, which stretches back to 1998.
Nevertheless, the experts will advise that consumers should reduce their daily red meat intake to 70g.
This is the current average across the whole population, but among those who eat red meat, consumption is likely to be considerably higher because an estimated six million people eat none, including 3.6 million vegetarians.
The experts will warn of particular risks to the third of the adult population consuming more than 100g a day. Current advice, which dates from 1998, suggested 90g a day was a healthy amount, and that people only needed to cut back on red meat if they were eating more than 140g every day.
Scientists believe a pigment found in red meat damages the DNA of cells lining the digestive system – and DNA damage is one of the first signs of cancer. Burning meat is also thought to increase the risks. In addition, some studies suggest that preservatives used in processed meat could increase risks.
Studies have also suggested links between red meat and heart disease and type 2 diabetes. Obesity increases the risks of many diseases, and some research has suggested that those who avoid red meat tend to weigh less.
Eating a vegetarian diet may reduce your overall risk of cancer, but increase your risk of bowel cancer, new research suggests.
The study, published in the American Journal of Clinical Nutrition, included 52,706 people aged between 20 and 89. Participants were recruited between 1993 and 1999, as part of the European Prospective Investigation into Cancer and Nutrition (EPIC) study, and followed until 2005.
They were separated into four groups: meat eaters, fish eaters, vegetarians and vegans. All cancer diagnoses and deaths were recorded using the National Health Service Central Register.
The overall number of cancer cases was lower in vegetarians and fish eaters than in meat eaters, adding to previous evidence which has shown that vegetarians are less likely to get cancer.
But surprisingly, the number of bowel (colorectal) cancer cases was higher in vegetarians than meat eaters, contradicting previous research. Dr Tim Key, one of the study authors, told Bupa’s health information team: “For colorectal cancer, our results are somewhat unexpected.
“Other studies have shown that people who eat a lot of meat may have a higher risk of colorectal cancer than people who eat small amounts of meat. We don’t know why our results are different. They may be giving a clue that we don’t fully understand the relationship of meat with this type of cancer.
“We are conducting further studies to look into this,” Dr Key added.
Heather Caswell, a nutrition scientist from the British Nutrition Foundation, thinks this is an interesting finding.
“When you look more closely at the detail of the study, it can be seen that the meat eaters were actually only eating moderate amounts of meat, which were well within what is recommended for a healthy diet. Further, both groups also had similar intakes of fruit and vegetables, with them both just about meeting the five-a-day target,” she said.
“This study highlights the fact that cancer is a complex disease and many different lifestyle factors play a part in determining an individual’s risk.”
The overall incidence of cancer in the study group was lower than the national average. “This is likely to be down to the fact that all the subjects in this study were fairly healthy – for example they were a healthy weight and the majority were non-smokers,” explained Heather Caswell.
“This suggests that an overall healthy diet, which may include moderate amounts of meat, and lifestyle help to reduce cancer risk,” she added.
Unfortunately, studies like this don’t prove that whole grains are responsible for the good health outcomes. It’s highly likely that people who choose to eat wholegrain foods are unique human beings and health conscious in all sorts of ways. They don’t smoke, they try to be physically active, they eat less red meat and more fruit and vegetables. Of course, good studies will statistically “adjust” for these confounders, as they are called. But I have a niggling feeling that not all the confounders may have been accounted for. Perhaps the person who chooses brown rice over white rice looks after their health in ways that are not yet recorded by researchers e.g. they eat more slowly, they breathe deeply and they get less stressed.
I get the same niggly feeling here too. Especially when I factor in the ineptitude of government researchers, who they have drawn on to come up with this information, and having some knowledge of how they collect data for these types of studies (someone would have answered a food frequency questionnaire years before the bowel cancer got them, and they would have said they eat pizza, which would have been categorised as red meat – I’m quite serious).
Not even their proposed mechanism seems to be irrefutable (it looks as though they are going to peg this one on iron causing DNA damage). I was going to do a post of its own regarding this, but it seems to fit here. I have previously posted about the meat-only derived compound carnosine;
Carnosine is a dipeptide which protects against aging, is a copper and zinc chelating agent, increases the lifespan of cells, is a pH buffer, assists in the contraction of the heart muscle, protects the brain from excitotoxins, and helps to prevent Alzheimer’s Disease (possibly through its extraction of heavy metals). Carnosine is only found in meat. Some vegetarians try to compensate with supplements, but such attempts are futile, due to the rate at which carnosine is used. When 248 mg. is consumed, it becomes untraceable within 5.5 hours. The minuscule synthetic 50 mg. supplements commonly used by vegetarians and vegans are useless.
Carnosine is a neuroprotective dipeptide consisting of β-alanine and L-histidine. It demonstrates a number of useful features, including stimulation of brain and muscle microcirculation and a rejuvenating effect on cultured cells. Its activity is based on its antioxidant and antiglycating action that, in addition to heavy metal chelation and pH-buffering ability, makes carnosine an essential factor for preventing neurodegeneration and accumulation of senile features. Recently, carnosine was successfully used to treat patients after brain stroke or patients with Parkinson disease. We conclude that carnosine can be recommended for patients under oxidative stress as a natural remedy having high efficiency and no side effects.
Carnosine is found in high concentrations in skeletal muscles, where it is involved in several physiological functions. The muscle carnosine content measured within a population can vary by a factor 4. The aim of this study was to further characterize suggested determinants of the muscle carnosine content (diet, gender and age) and to identify new determinants (plasma carnosinase activity and testosterone). We investigated a group of 149 healthy subjects, which consisted of 94 men (12 vegetarians) and 55 women. Muscle carnosine was quantified in M. soleus, gastrocnemius and tibialis anterior using magnetic resonance proton spectroscopy and blood samples were collected to determine CNDP1 genotype, plasma carnosinase activity and testosterone concentrations. Compared to women, men have 36, 28 and 82% higher carnosine concentrations in M. soleus, gastrocnemius and tibialis anterior muscle, respectively, whereas circulating testosterone concentrations were unrelated to muscle carnosine levels in healthy men. The carnosine content of the M. soleus is negatively related to the subjects’ age. Vegetarians have a lower carnosine content of 26% in gastrocnemius compared to omnivores. In contrast, there is no difference in muscle carnosine content between omnivores with a high or low ingestion of β-alanine. Muscle carnosine levels are not related to the polymorphism of the CNDP1 gene or to the enzymatic activity of the plasma carnosinase. In conclusion, neither CNDP1 genotype nor the normal variation in circulating testosterone levels affects the muscular carnosine content, whereas vegetarianism, female gender and increasing age are the factors associated with reduced muscle carnosine stores.
Perhaps increasing age is a factor due to changes in dentition over time making it harder for older people to chew meat, the cost of meat being prohibitive to those on a fixed retirement income or living in an institutionalised home that is trying to keep costs down and profits up, and/or the fact that many oldies get to a point where they start to fear their own mortality a bit more (have had a few friends die) and try to buy themselves some more time by ‘eating healthy’.
Hopefully you can see from the above and my previous post on the topic, that carnosine (FROM MEAT) is incredibly important to health. But how does any of the above relate carnosine to colorectal cancer. Easy – via the next paper I want to discuss.
Iron is likely to be fingered as the driving agent for colorectal cancer. Iron can be a pro-oxidant and as such, may cause free-radical production and DNA damage. This may lead to tumor cell growth and proliferation. Fortunately, the body has several mechanisms in place to protect against this happening… and one of those systems utilises carnosine… did I mention it is from meat?
Protective effects of carnosine and homocarnosine on ferritin and hydrogen peroxide-mediated DNA damage.
Previous studies have shown that one of the primary causes of increased iron content in the brain may be the release of excess iron from intracellular iron storage molecules such as ferritin. Free iron generates ROS that cause oxidative cell damage. Carnosine and related compounds such as endogenous histidine dipetides have antioxidant activities. We have investigated the protective effects of carnosine and homocarnosine against oxidative damage of DNA induced by reaction of ferritin with H(2)O(2). The results show that carnosine and homocarnosine prevented ferritin/H(2)O(2)-mediated DNA strand breakage. These compounds effectively inhibited ferritin/H(2)O(2)-mediated hydroxyl radical generation and decreased the mutagenicity of DNA induced by the ferritin÷H(2)O(2) reaction. Our results suggest that carnosine and related compounds might have antioxidant effects on DNA under pathophysiological conditions leading to degenerative damage such as neurodegenerative disorders.
So this paper highlights that carnosine has antioxidant effects, though it looks at this with specific regard to the neurological system (nice to know that meat is protecting my brain). Could carnosine have the same effect on the intestinal cells? Yep…
Characterization of carnosine uptake and its physiological function in human intestinal epithelial Caco-2 cells.
Carnosine (beta-Ala-L-His) is known to have the physiological functions of an antioxidant. Although dietary carnosine is thought to be absorbed across intestinal epithelial cells, the mechanism for this absorption is not yet well understood and its function in the intestinal tract is also obscure. The intestinal transport of carnosine was characterized in the present study by using human intestinal Caco-2 cells, and its physiological function in these cells was further examined. The carnosine uptake was proton-dependent, being activated by lowering the apical pH value. Its uptake was significantly inhibited by other dipeptides, whereas it was not inhibited by other amino acids. These characteristics of the carnosine uptake strongly suggest its transport into the cells via peptide transporter 1 (PepT1). Since carnosine has antioxidative activity, we studied its effect on the H2O2-induced secretion of inflammatory cytokines in Caco-2 cells. The H2O2 induced increase in IL-8 secretion was inhibited by a pretreatment with carnosine for 3 h, this inhibition being presented in a dose-dependent manner. These results suggest that carnosine had a protective effect against oxidative stress in intestinal epithelial cells.
The cells they refer to here, Caco-2 cells, are colorectal adenocarcinoma cells – derived from colon cancers. So look at our lines of evidence for a biological mechanism that would directly support a high level of red meat consumption causing colorectal cancer… a study has shown it (colorectal cancer) is as likely to occur in vegetarian’s, and we have a study that shows a compound derived from meat is likely protective against the type of oxidative damage that iron could do. Not looking too good then for the scientists who are claiming all swans are white is it?
Let’s throw another couple of confounders into the mix shall we, just to confuse things even more…
Iron and colorectal cancer risk: human studies.
Some reports have associated iron with cancer risk, particularly of the colorectum. This review will focus on the human studies that have investigated this association. Comparative studies were sought in which people with and without colorectal neoplastic lesions, either cancers or adenomatous polyps, were assessed for iron exposure. Iron exposure variables included dietary iron intake, iron vitamin supplementation, body iron stores as measured by ferritin or transferrin saturation, and gene status for hereditary hemochromatosis. Medline was searched for published reports using the key words iron, cancer, colon, rectum, ferritin, transferrin, and hemochromatosis. In addition, the Cochrane Library was searched for relevant studies and several authors were contacted to investigate their awareness of unpublished studies. Studies were categorized by study design and ranked for quality of innovation in design, sample size, and thoroughness of iron status ascertainment. Thirty-three studies were reviewed in 26 publications. Of the larger studies, approximately three-quarters supported the association of iron, in all three strata of exposure, with colorectal neoplasia risk. Because iron is broadly supplemented in the American diet, the benefits of iron supplementation need to be measured against the long-term risks of increased iron exposure, one of which may be increased risk of colorectal cancer.
Whoa… now I didn’t recall anything from the boffins suggesting that we need to eat only one steak per week saying anything about iron supplements or a hereditary iron overload disease increasing the risk! Did you?
Iron overload gene tied to colon cancer increased risk
Researchers at the University of North Carolina at Chapel Hill School of Medicine have found that people with gene mutations associated with abnormally high iron levels are 40 percent more likely than others to develop colon cancer.
A report of the research published in the Journal of the National Cancer Institute found the cancer risk greater in mutation carriers who are older or who consume high quantities of iron.
“Our findings are consistent with the view that taking in too much iron may be an environmental risk factor for colon cancer in some people,” said study lead author Dr. Nicholas J. Shaheen, assistant professor of medicine and assistant professor of epidemiology in the UNC School of Public Health.
Iron is a pro-oxidant, thus high iron levels can lead to free radical formation and DNA damage, said Shaheen and co-authors. The authors added that iron is an essential element for tumor cell growth and proliferation.
People inherit two copies of a gene known as HFE, one from each parent. Mutations to the gene are common, occurring in an estimated 15 percent of the U.S. population, Shaheen said. Two such mutations investigated in the study are strongly associated with the development of hereditary hemochromatosis, a condition characterized by iron overload and that leads to problems of the pancreas, liver, heart and other organs. The gene itself encodes a cellular signaling protein that plays a role in iron metabolism.
“We don’t fully understand why some people develop colon cancer and others do not,” Shaheen said. “Our goal was to look for genetic risk factors for the disease that might be easily identifiable.”
Thirteen hundred adults, ages 40 through 79, were involved in this population-based case-control study, including people with and without colon cancer. Participants provided information on total iron intake and use of non-steroidal anti-inflammatory drugs (NSAIDs). Blood samples were provided, and DNA was extracted and analyzed for two major HFE gene mutations.
After controlling for age, race, gender, red meat consumption, NSAID use and total iron intake, study participants with any HFE gene mutation were found to be 1.4 times more likely to have colon cancer than participants with no HFE gene mutation. The risk of colon cancer associated with an HFE mutation was similar for those who did and did not have a family history of colon cancer. And among people with HFE mutations, cancer risk increased with increasing age and with total iron intake.
“When you have a high number of people with the mutation, and although the mutation itself confers only a mildly increased risk, the total number of cancers that may be attributed to HFE mutations could be fairly high,” Shaheen said.
Given the relatively high numbers of people in the population with the HFE mutations, and the other target organs that are impacted (pancreas = diabetes, heart = heart disease…), is this where we see our links between red meat and these other diseases? Could the inconsistent numbers be all over the show depending on how many people with iron overload you end up with in your study cohort? Then we have to factor in the high level use of iron supplements. Iron deficiency, ironically, is one of the most common deficiencies (don’t get me started on why that might be…. hint: GRAINS and fear of red meat), so iron supplementation is incredibly common. Can other factors mitigate the effects of having the gene mutation, such as increased antioxidant support from vegetables… or that plant matter might in fact bind some of the iron up in the gut, preventing it from acting as a pro-oxidant?
I could probably spend many, many hours trying to search the literature to come up with some answers to these questions. But then why the hell should I? Wouldn’t you expect that the people issuing public health guidelines have done all this homework already? All of this should be answered before taking the step of asking the public to massively restrict their red meat intake. And what happens in a few years time when we have even higher rates of dementia going on due to rampant carnosine deficiencies? Who picks up the pieces on that one?
Look, at the end of the day, I am a very amateur blogger. If I can, in the space off an evening, dig up enough to confound and put holes in the argument to consume less red meat, there is something seriously up. The people making these claims need to stop treating the public like they are idiots (some of us aren’t) and stump up with their evidence with full disclosure for others to look at and robustly debate, BEFORE issuing media releases (prior to the release of any report) that call for very major dietary changes. We have been down this path before with the whole cholesterol nonsense. And quite frankly, it gets very tiresome having to defend and justify to people why I back a few million years of evolution over some numpties in a government department in old Blighty.
Extra for experts: More on iron metabolism here. One can easily see there is more to it than just not eating red meat (for example, amenorrheic women will have iron accumulate if they are not having a regular period… as will post-menopausal women, and women are more likely to take supplemental iron).
– Bowel cancer is the second most common type of cancer in women
– Almost three-quarters of people with bowel cancer are diagnosed when they are 65 or over.