Remember the basic four food groups?
Beth Dixon, Ph.D., from the Department of Nutrition of New York University is going to try to talk about Dietary Guidelines for Americans (but it sounds like she's got a sore throat).
Out of the 2005 Dietary Guidelines for Americans, she says, came a focus on consuming a variety of foods, controlling calorie intake, increasing fruits and vegetables, etc. We know all this, but what was new was the USDA Food Guide (based on MyPyramid) and the DASH eating plan.
The USDA Food Guide were designed to be flexible with 12 different plans at a 2000-calorie level with main food groups (like fruits, vegetables) given in amounts (like 2 cups per day). There are also subgroup categories such as vegetables having a subgroup of dark green vegetables, orange vegetables, etc.
"The idea behind these food plans is to focus on nutrient-dense foods," she says. "There's a behind-the-scenes way of counting food groups."
To get to the concept of diet quality, the USDA folks developed a Healthy Eating Index. It's based on the idea that there is some way to measure diet quality that assesses adherence to a diet plan. Again, like other indices, it has weighted scoring of various foods.
There have also been recent revisions to the HEI such as "SoFAAS" (which we'll keep hearing about) that represents solid fats, alcohol and added sugars.
She goes on with a highlight of Guenther et al. data in Nutrition Insight on NHANES showing that there is a significantly lower intake of whole fruits and whole grains, higher dairy (mostly cheese).
And she also looks at Krebs-Smith et al (J Ntr 2010) data showing that many Americans do not meet dietary recommendations.
More studies... (my wrists hurt)
There are lots of total diet indices that show that a better quality diet is associated with better markers in cardiovascular disease.
Stay tuned for 2010 Dietary Guidelines for Americans with updates to the HEI. A direct quote from the new guide, "Recommended intake amounts in the USDA Food pattern remains unchanged from 2005 with the exception of the vegetable subgroups [red orange veg and cooked dry beans and peas]."
She's closing now... whew! ... with Reedy et al data from 2010 Am J Prev med on The Food Environment. Looks like it's in a typical American environment you can potentially find it easy to eat whole grains, but harder in other areas like fruits and vegetables.
Showing posts with label American College of Nutrition. Show all posts
Showing posts with label American College of Nutrition. Show all posts
08 October 2010
Nutrition and Chronic Disease with Nicola McKeown
Next up at American College of Nutrition conference, we're about to enjoy a talk given on "Nutrition and Chronic Disease: Advantages of a Diet Pattern and Health Outcomes" given by Nicola M. McKeown, Ph.D., of the USDA Human Nutrition Research Center on Aging at Tufts University.
"Trying to measure dietary exposures is very difficult," sayd McKeown. The nature of nutrition is extremely complex, and she quotes Walter Willet on the complexity (which makes me like her already). "A single nutrient may be confounded by an overall dietary pattern."
Single-nutrient approaches ignore complexity of diets, biological interactions, and there is difficulty to detect small effects and observe health effects of single components.
How do we research with this complexity? We may be interested in a dietary pattern, a food group, an individual food, single nutrients, and bioactives (a top-down approach).
Why study dietary patterns? They represent the interactions and cumulative effects of dietary components on disease risk. They capture potential foods and nutrient synergy. They help generate hypotheses about biological mechanisms, and they can translate to dietary pattern recommendations.
In epidemiology, there are two ways to derive dietary pattern approaches are theoretical (hypothesis-oriented) and empirical (exploratory-oriented). "The data drives the patterns," she says. Most of the time it's based on food frequency questionnaires. The input variables may be frequency, weight, daily percent of energy contribution.
With a factor analysis, the goal is to identify common factors that explain variance in the dietary data. it's based on correlation/covariance matrix of the food groups. It aggregates specific food groups on the basis of degree of use.
She then shows examples where various food groups are weighted based on factor loading of top contributing foods. A Western dietary pattern, for example, is higher in meat, processed meat, and butter in comparison to a prudent dietary pattern.
Cluster analysis (which you may "hear a lot about in the literature") is based on aggregates of individuals into distinct food groups. It's sensitive to extreme outliers so treatment of input variables is important.
She gives a few examples of cluster analysis, such as:
Cluster 1: reduced-fat dairy, fruits, and whole-grains.
Cluster 2: refined grains and sweets.
Cluster 3: Beer (lots of men were in this category).
Cluster 4: Soda (people in this category were found to have higher fasting insulin)
From a research standpoint, there have been a few diets with great interest including the Mediterranean diet and low-carb diet. There have been indexes developed for these two diets as well as the Healthy Eating Index.
The indexes can be used to create a "diet score," each of which are based on cut-points of various food groups with criteria that determine weight of each food that contribute to the score. [The diet scores look like a handy tool for helping people stay on track.]
The 2005 Dietary Guidelines for Americans Adherence Index (DGAI) are based on food intake recommendations and it penalizes for overconsumption of discretionary energy and energy-dense foods (chips and French fries). They also had a "variety score" when people had various foods in the diet.
When individuals adhere to the DGAI, they had a lower prevalence of metabolic syndrome. Based on the scoring approach, McKeown says, it's possible for people to get the same score and have different dietary patterns.
Regarding the Mediterranean dietary pattern, McKeown reminds us that "there is no single Mediterranean diet," but it's based on patterns, so a diet score can be useful for adhering to the dietary pattern.
When discussing low-carb dietary patterns, they have similar macronutrient composition, but may have different dietary quality. There should be scores indicated depending on the choices of fat -- animal or vegetable. She is careful to note that it's important to consider that when you talk about macronutrients to consider substitutions for foods eliminated.
She closes by saying that there is subjectivity in defining cut points in indices. Indices may be a good index of diet quality but not of disease risk. High scores are rare, but average scores can be achieved a number of different ways. Eating patterns associate with other health behaviors.
Helping the Brain Help Itself keynote by Mark Mattson
Now, for the second keynote at American College of Nutrition conference in New York City we're listening to Mark Mattson, Ph.D. He starts out talking about his work in the laboratory of neurosciences at National Institutes of Aging.
He talks about what happens during aging in the brain.
More and more as people get older, neurons age and die, predisposing us to Alzheimer's and other brain diseases. The mechanisms on how this happens are being shown and he discusses the different pathways.
Dietary energy restriction, exercise, cognitive enrichment promote neuroprotection (hormesis?) by reducing oxidative stress and inflammation.
Current trends in Alzheimer's showing it's a huge issue that's not being dealt with. We need a war on it like we have on cancer. Many people die from Alzheimer's and it's a tax on society.
He discusses amyloid plaques and neurofibrillary tangles (with tau) that is involved in AD pathogenesis.
There's a number of animal models for AD such as transgenic mice with overexpression of mutated amyloid-precursor protein. Also, PS1 mice.
Mattson manipulates diets of AD-prone mice to see how diet affects their cognitive function, memory, and amelioration of AD behavior.
Intermittent fasting and calorie restriction ameliorated AD behavior changes. He thinks that neurons can be stimulated by these diets to protect themselves against the amyloid protein. He shows us data on how CR reduced tau levels, but IF did not.
They also used "couch potato mice" model of AD: overfed, sedentary. Of course, these are great controls.
CR and IF showed gene expression in the brain (Martin et al, 2007, Endocrinology).
They wanted to show an effect in primates, so performed a study in rhesus monkeys. They took the monkeys and reduced their calories by 30 percent for 11 months. They tested their motor function, dopamine. They injected a toxin called MPTP.
Both the animals on the normal diet and CR diet had deficits in motor function, but CR had less seeming to have a protective effect from a functional endpoint. When measured for dopamine, there was major depletion in the striatum in both. When measured for BDNF, the CR had higher levels of BDNF.
In a stroke model, they took young, middle-aged, or old mice on either IF or normal diets. They then damaged the cerebral cortex and measured neurological deficit. There was significant benefit for the young and middle-aged mice on IF, but not in old.
"So start early," he says. Exercise, eat less when you're younger to prevent Alzheimer's in the future. IF reduced inflammation in the young and middle-aged, but not in old.
Mattson starts talking about type 2 diabetes now. The world prevalence of diabetes is rising. This disease leads to problems later on in the brain, as shown in more mice models (like leptin-receptor mutant mice), which he summarizes.
- reduced BDNF levels
- l wer neurogenesis
Diabetes reduces neurogenesis, but what about interactions with exercise or calorie restriction? Both exercise and CR increase BDNF levels.
Mattson talking about possibility of using drugs and phytochemicals now (Duen et al 2004; Nelson et al 2007).
Some drugs work by involving BDNF. There are also several fruits and vegetables, but he doesn't think they have an intrinsic factor as antioxidants. Instead, he said, they have toxins concentrated in the skin meant to repel insects. Lots of these plants have natural pesticides, so Mattson acquired many of these natural chemicals to see which produce resistance to neurogenerative disorders.
OK, back to talking about IF, this time about a study showing that IF improves cardiovascular risk factors under stress in animals.
-The body temperature is up on the feeding day, down low on the fasting day.
-Heart rate variability was measured too. Higher heart rate variability is a good thing, because it shows adaptability. IF improved heart rate variability.
-Higher levels of BDNF
Interesting thing, he notes, when they infused BDNF in mice, they showed better heart rate variability.
Human studies? Mattson talks of Jim Johnson's work on subjects with moderate asthma on alternate-day calorie restriction. The subjects adapted to the diet, lost bodyweight, their mood increased, but importantly their asthma improved.
Mattson begins discussing GLP1, a receptor that when stimulated reduces amyloid plaque accumulation, and drugs that stimulate it. GLP1 increases BDNF and insulin sensitivity.
He intends to conduct a 3-year double-blind, randomized trial on a drug (Exendin-4) to treat Alzheimer's disease, by testing CSF biomarkers. He is optimistic and says at least he knows the drug should help with blood glucose management.
---
Unfortunately, Mattson ran out of time, but the presentation was awesome! Good to know we have serious scientists like this working on AD.
Surprisingly, with all the talk about CR, IF and Alzheimer's, not a word was said about Sirtuin 1 activation, so I asked Dr. Mattson his opinion on the research, specifically Guarente's paper showing that SIRT1 activation inhibited two pathways in the progression of AD.
Mattson responded with a dose of skepticism about sirtuins and their potential, at least as a treatment in the diseased state when they'd use up a lot of NADPH at a time when the brain needs it.
hmm...
He talks about what happens during aging in the brain.
More and more as people get older, neurons age and die, predisposing us to Alzheimer's and other brain diseases. The mechanisms on how this happens are being shown and he discusses the different pathways.
Dietary energy restriction, exercise, cognitive enrichment promote neuroprotection (hormesis?) by reducing oxidative stress and inflammation.
Current trends in Alzheimer's showing it's a huge issue that's not being dealt with. We need a war on it like we have on cancer. Many people die from Alzheimer's and it's a tax on society.
He discusses amyloid plaques and neurofibrillary tangles (with tau) that is involved in AD pathogenesis.
There's a number of animal models for AD such as transgenic mice with overexpression of mutated amyloid-precursor protein. Also, PS1 mice.
Mattson manipulates diets of AD-prone mice to see how diet affects their cognitive function, memory, and amelioration of AD behavior.
Intermittent fasting and calorie restriction ameliorated AD behavior changes. He thinks that neurons can be stimulated by these diets to protect themselves against the amyloid protein. He shows us data on how CR reduced tau levels, but IF did not.
They also used "couch potato mice" model of AD: overfed, sedentary. Of course, these are great controls.
CR and IF showed gene expression in the brain (Martin et al, 2007, Endocrinology).
They wanted to show an effect in primates, so performed a study in rhesus monkeys. They took the monkeys and reduced their calories by 30 percent for 11 months. They tested their motor function, dopamine. They injected a toxin called MPTP.
Both the animals on the normal diet and CR diet had deficits in motor function, but CR had less seeming to have a protective effect from a functional endpoint. When measured for dopamine, there was major depletion in the striatum in both. When measured for BDNF, the CR had higher levels of BDNF.
In a stroke model, they took young, middle-aged, or old mice on either IF or normal diets. They then damaged the cerebral cortex and measured neurological deficit. There was significant benefit for the young and middle-aged mice on IF, but not in old.
"So start early," he says. Exercise, eat less when you're younger to prevent Alzheimer's in the future. IF reduced inflammation in the young and middle-aged, but not in old.
Mattson starts talking about type 2 diabetes now. The world prevalence of diabetes is rising. This disease leads to problems later on in the brain, as shown in more mice models (like leptin-receptor mutant mice), which he summarizes.
- reduced BDNF levels
- l wer neurogenesis
Diabetes reduces neurogenesis, but what about interactions with exercise or calorie restriction? Both exercise and CR increase BDNF levels.
Mattson talking about possibility of using drugs and phytochemicals now (Duen et al 2004; Nelson et al 2007).
Some drugs work by involving BDNF. There are also several fruits and vegetables, but he doesn't think they have an intrinsic factor as antioxidants. Instead, he said, they have toxins concentrated in the skin meant to repel insects. Lots of these plants have natural pesticides, so Mattson acquired many of these natural chemicals to see which produce resistance to neurogenerative disorders.
OK, back to talking about IF, this time about a study showing that IF improves cardiovascular risk factors under stress in animals.
-The body temperature is up on the feeding day, down low on the fasting day.
-Heart rate variability was measured too. Higher heart rate variability is a good thing, because it shows adaptability. IF improved heart rate variability.
-Higher levels of BDNF
Interesting thing, he notes, when they infused BDNF in mice, they showed better heart rate variability.
Human studies? Mattson talks of Jim Johnson's work on subjects with moderate asthma on alternate-day calorie restriction. The subjects adapted to the diet, lost bodyweight, their mood increased, but importantly their asthma improved.
Mattson begins discussing GLP1, a receptor that when stimulated reduces amyloid plaque accumulation, and drugs that stimulate it. GLP1 increases BDNF and insulin sensitivity.
He intends to conduct a 3-year double-blind, randomized trial on a drug (Exendin-4) to treat Alzheimer's disease, by testing CSF biomarkers. He is optimistic and says at least he knows the drug should help with blood glucose management.
---
Unfortunately, Mattson ran out of time, but the presentation was awesome! Good to know we have serious scientists like this working on AD.
Surprisingly, with all the talk about CR, IF and Alzheimer's, not a word was said about Sirtuin 1 activation, so I asked Dr. Mattson his opinion on the research, specifically Guarente's paper showing that SIRT1 activation inhibited two pathways in the progression of AD.
Mattson responded with a dose of skepticism about sirtuins and their potential, at least as a treatment in the diseased state when they'd use up a lot of NADPH at a time when the brain needs it.
hmm...
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