NUTRISPEAK by Vesanto Melina

TEACHERS IN our schools are supplied with a multitude of resources from the closely aligned meat and dairy industries. These materials are designed to establish in children’s minds the idea that we must eat meat to obtain iron and that cow’s milk is essential for bone building in humans. Neither of these industry-derived fabrications is true, but if you are still haunted by these rusty facts, read the solid update concerning iron that follows. (See next month’s column for an update on calcium.)

Iron is a "precious metal" when it comes to human health. as part of our blood cells, it plays a central role in transporting oxygen throughout the body, releasing this life-giving sub-stance where needed and carrying away the metabolic waste product carbon dioxide. as part of many enzyme systems, iron also plays key roles in the production of cellular energy, immune system functioning and in the mental processes surrounding learning and behaviour.

Every day, we lose miniscule amounts of iron in cells that are sloughed from skin and intestinal walls. We recycle our body’s iron supply and those losses must be replaced. Women of childbearing age lose additional iron during menstruation. The building of new cells can deplete the small reserves of infants and children. with teens, there can be the double challenge of growth and notoriously poor eating habits (though vegetarian teens tend to eat better than non-vegetarian teens). The most prevalent nutritional deficiency in North America is that of iron and the most susceptible groups are women of childbearing age, teens and young children.

Naturally, those who experience blood loss for any reason – people with ulcers or blood donors – have increased needs and athletes have high requirements due to increased oxygen demands.

Symptoms of iron deficiency include exhaustion, sensitivity to cold, irritability and pale skin. (These symptoms may have other causes as well.) If you have doubts about your iron status, have your hemoglobin, serum iron and transferrin (iron transport protein) checked.

Iron deficiency anemia is no more common among vegetarians than non-vegetarians. While iron from plant foods is not absorbed as well as the iron from meat, vegetarian diets tend to be higher in iron and far higher in the vitamin C that helps us absorb iron from plant foods. Vegans consume even more iron and tend to replace milk, which contains no iron and also inhibits iron absorption, with iron-rich foods such as soymilk. Oranges or orange juice help us absorb iron from the tofu or soymilk in a smoothie. Sweet red pepper helps us absorb iron from chickpeas, beans, lentils or soy foods in the same meal. Kiwifruit, papaya and salad help us absorb iron from nuts, whole grains or beans when eaten at approximately the same time.

Food preparation techniques can also increase our iron absorption. These include soaking beans prior to cooking; the sprouting of grains, seeds and legumes; the leavening of whole grain breads; and the fermenting of tempeh or miso. Surprisingly, cast-iron or stainless steel cookware can contribute to our iron supply when we cook acidic foods such as spaghetti sauce or sweet and sour sauce. On the other hand, our absorption of iron is reduced when we drink black or green teas or cow’s milk with iron-containing meals. To get more iron, drink water or fruit juices that contain vitamin C with your meals.

Strike it rich with iron from plant foods

Here are some tips to maximize the iron in your diet:

1. Eat iron-rich plant foods (especially beans, peas and lentils).
2. Use iron-fortified foods (enriched cereals, grain products and meat analogues) and whole grains.
3. Help your body absorb iron by eating foods rich in vitamin C at the same time.
4. Use foods that are leavened, sprouted, soaked (as with beans) and fermented.
5. If your iron status is low, avoid consuming dairy products and black or green teas at the same time as iron sources.
6. Use cast-iron or stainless steel cookware.
7. If in doubt, have your iron status checked.

Vesanto Melina is a dietitian and author based in Langley, BC. after being in writer’s hibernation for the last six months, she resumes offering consultations in mid-May. 604-882-6782.

posted by Adam on 21 Feb 2011 at 10:06 am

This is a terrible study, and worse, the media is making false statements which are nowhere to be found in the study. This was a study of people who were “tired” or “depressed,” and intentionally restricted the sample. This was a purely political study financed by insurance and by government.Most people with CFS find out their limitations and understand what level of activity they can withstand without relapsing.CFS patients have 30% less blood volume, have marked mitochondrial dysfunction, both of which can lead to congestive heart failure. They have multiple co-infections with herpesviruses EBV, CMV, HHV and often have others such as pathgenic mycoplasma, chlamydia pneumoniae, and intrusion of enteric bacteria into the blood due to high levels of inflammatory cytokines. They have high antibodies to many bacterias and viruses at levels which healthy people just do not have. Their RNaseL enzyme system is engaged at fighting viral replicated at levels healthy people just don’t have, and it borrows from the cellular energy needed to maintain normal levels of activity.Telling CFS patients to exercise their way out of illness makes about as much sense as telling a person with a severe cold to get on an exercise bike and go really fast until they get better.They have marked irregularities in cytokines, abnormalities in natural killer cell counts, and markedly decreased natural killer cell cytotoxicity. CFS patients can lose nearly all of their ability to kill latent viruses — scoring worse than HIV/AIDS patients. by contrast, severe depression combined with smoking has a small fraction of the effect on the immune system.

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(SACRAMENTO, Calif.) — Children with autism are far more likely to have deficits in their ability to produce cellular energy than are typically developing children, a new study by researchers at UC Davis has found. The study, published today in the Journal of the American Medical Association (JAMA), found that cumulative damage and oxidative stress in mitochondria, the cells energy producer, could influence both the onset and severity of autism, suggesting a strong link between autism and mitochondrial defects.

After the heart, the brain is the most voracious consumer of energy in the body. The study’s authors propose that deficiencies in the ability to fuel brain neurons might lead to some of the cognitive impairments associated with autism. Mitochondria are the primary source of energy production in cells and carry their own set of genetic instructions, mitochondrial DNA (mtDNA), to carry out aerobic respiration. Dysfunction in mitochondria already is associated with a number of other neurological conditions, including Parkinsons disease, Alzheimers disease, schizophrenia and bipolar disorder.

Children with mitochondrial diseases may present exercise intolerance, seizures and cognitive decline, among other conditions. some will manifest disease symptoms and some will appear as sporadic cases, said Cecilia Giulivi, the studys lead author and professor in the Department of Molecular Biosciences in the School of Veterinary Medicine at UC Davis. many of these characteristics are shared by children with autism.

The researchers stress that these new findings, which may help physicians provide early diagnoses, do not identify the cause or the effects of autism, which affects as many as 1 in every 110 children in the United States, according to the U.S. Centers for Disease Control and Prevention.

While previous studies have revealed hints of a connection between autism and mitochondrial dysfunction, these reports have been either anecdotal or involved tissues that might not be representative of neural metabolism.

“It is remarkable that evidence of mitochondrial dysfunction and changes in mitochondrial DNA were detected in the blood of these young children with autism,” said Geraldine Dawson, chief science officer of Autism Speaks, which provided funding for the study. “One of the challenges has been that it has been difficult to diagnose mitochondrial dysfunction because it usually requires a muscle biopsy. If we could screen for these metabolic problems with a blood test, it would be a big step forward.”

For the study, Giulivi and her colleagues recruited 10 autistic children aged 2 to 5, and 10 age-matched typically developing children from similar backgrounds. The children were randomly selected from Northern California subjects who previously had participated in the 1,600-participant Childhood Autism Risk from Genetics and the Environment (CHARGE) Study and who also consented to return for a subsequent study known as CHARGE-BACK, conducted by the UC Davis Center for Childrens Environmental Health and Disease Prevention.

The children with autism met stringent diagnostic criteria for autism as defined by the two most widely used and rigorous assessment tools. Though the total number of children studied was small, it is generally representative of the much larger CHARGE cohort and that increases the significance of the study results, the authors said.

The researchers obtained blood samples from each child and analyzed the metabolic pathways of mitochondria in immune cells called lymphocytes. Previous studies sampled mitochondria obtained from muscle, but the mitochondrial dysfunction sometimes is not expressed in muscle. Muscle cells can generate much of their energy through anaerobic glycolysis, which does not involve mitochondria. by contrast, lymphocytes, and to a greater extent brain neurons, rely more heavily on the aerobic respiration conducted by mitochondria.

The researchers found that mitochondria from children with autism consumed far less oxygen than mitochondria from the group of control children, a sign of lowered mitochondrial activity. For example, the oxygen consumption of one critical mitochondrial enzyme complex, NADH oxidase, in autistic children was only a third of that found in control children.

A 66 percent decrease is significant, Giulivi said. When these levels are lower, you have less capability to produce ATP (adenosine triphosphate) to pay for cellular work. Even if this decrease is considered moderate, deficits in mitochondrial energy output do not have to be dismissed, for they could be exacerbated or evidenced during the perinatal period but appear subclinical in the adult years.

Reduced mitochondrial enzyme function proved widespread among the autistic children. eighty percent had lowered activity in NADH oxidase than did controls, while 60 percent, 40 percent and 30 percent had low activity in succinate oxidase, ATPase and cytochrome c oxidase, respectively. The researchers went on to isolate the origins of these defects by assessing the activity of each of the five enzyme complexes involved in mitochondrial respiration. Complex I was the site of the most common deficiency, found in 60 percent of autistic subjects, and occurred five out of six times in combination with Complex V. Other children had problems in Complexes III and IV.

Levels of pyruvate, the raw material mitochondria transform into cellular energy, also were elevated in the blood plasma of autistic children. this suggests the mitochondria of children with autism are unable to process pyruvate fast enough to keep up with the demand for energy, pointing to a novel deficiency at the level of an enzyme named pyruvate dehydrogenase.

Mitochondria also are the main intracellular source of oxygen free radicals. Free radicals are very reactive species that can harm cellular structures, including DNA. Cells are able to repair typical levels of such oxidative damage. Giulivi and her colleagues found that hydrogen peroxide levels in autistic children were twice as high as in normal children. as a result, the cells of children with autism were exposed to higher oxidative stress.

Mitochondria often respond to oxidative stress by making extra copies of their own DNA. The strategy helps ensure that some normal genes are present even if others have been damaged by oxidation. The researchers found higher mtDNA copy numbers in the lymphocytes of half of the children with autism. These children carried equally high numbers of mtDNA sets in their granulocytes, another type of immune cell, demonstrating that these effects were not limited to a specific cell type. Two of the five children also had deletions in their mtDNA genes, whereas none of the control children showed deletions.

Taken together, the various abnormalities, defects and levels of malfunction measured in the mitochondria of autistic children imply that oxidative stress in these organelles could be influencing autisms onset.

The various dysfunctions we measured are probably even more extreme in brain cells, which rely exclusively on mitochondria for energy, said Isaac Pessah, director of the Center for Childrens Environmental Health and Disease Prevention, a UC Davis MIND Institute researcher and professor of molecular biosciences at the UC Davis School of Veterinary Medicine.

Giulivi cautions that these findings do not amount to establishing a cause for autism.

We took a snapshot of the mitochondrial dysfunction when the children were 2-to-5 years old. Whether this happened before they were born or after, this study cant tell us, she said.  however, the research furthers the understanding of autism on several fronts and may, if replicated, be used to help physicians diagnose the problem earlier.”

Pediatricians need to be aware of this issue so that they can ask the right questions to determine whether children with autism have vision or hearing problems or myopathies, Giulivi said. Exercise intolerance in the form of muscle cramps during intensive physical activity is one of the characteristics of mitochondrial myopathies.

The chemical fingerprints of mitochondrial dysfunction also may hold potential as a diagnostic tool. Giulivi and colleagues are now examining the mitochondrial DNA of their subjects more closely to pinpoint more precise differences between autistic and non-autistic children.

If we find some kind of blood marker that is consistent with and unique to children with autism, maybe we can change the way we diagnose this difficult-to-assess condition, she said.

The study also helps refine the search for autisms origins.

The real challenge now is to try and understand the role of mitochondrial dysfunction in children with autism, Pessah said. For instance, many environmental stressors can cause mitochondrial damage. Depending on when a child was exposed, maternally or neonatally, and how severe that exposure was, it might explain the range of the symptoms of autism.

“This important exploratory research addresses in a rigorous way an emerging hypothesis about potential mitochondrial dysfunction and autism,” said Cindy Lawler, program director at the National Institute of Environmental Health Sciences (NIEHS), which provided funding for the study. “Additional research in this area could ultimately lead to prevention or intervention efforts for this serious developmental disorder.”

Other study authors include Yi-Fan Zhang, Alicja Omanska-Klusek, Catherine Ross-Inta, Sarah Wong, Irva Hertz-Picciotto and Flora Tassone of UC Davis.

Funding for the study was provided by a UC Davis MIND Institute Pilot Research Grant, the National Institute of Environmental Health Sciences (NIEHS), the U.S. Environmental Protection Agency and Autism Speaks, including an Environmental Innovator Award from Autism Speaks.

The UC Davis MIND Institute in Sacramento, CA, was founded in 1998 as a unique interdisciplinary research center where parents, community leaders, researchers, clinicians and volunteers work together toward a common goal: researching causes, treatments and eventual preventions and cures for neurodevelopmental disorders. The institute has major research efforts in autism, Tourette syndrome, fragile X syndrome, chromosome 22q11.2 deletion syndrome and attention-deficit/hyperactivity disorder (ADHD). More information about the institute including previous presentations in its Distinguished Lecturer Series, is available on the Web at mindinstitute.ucdavis.edu/.