ALS Prevention Diet
I’m Elizabeth Brown, The Kitchen Vixen, a Registered Dietitian & Certified Holistic Chef. In 1988 I began my career path to become a Dietitian with the intent to one day host a healthy cooking show. As The Kitchen Vixen, I want to save the world by teaching people how to make life-saving recipes using health-promoting ingredients and preparation techniques which make the best use of someone’s time, energy, and financial resources. My adventures have taken me to many places in the US where I have had the opportunity to educate both personal clients as well as television viewers.
One of the most difficult years during my journey was in 2006 while living in Las Vegas. Initially I moved there to host a “LIVE” and internet based cooking show, but things went terribly wrong when I became involved with a very horrible individual.
However, for as much as I was having a difficult time living in Las Vegas, my trials where nothing compared to my friend June’s. Around the time I met June, while working in a physical therapy rehab hospital, June learned that her new husband Les was diagnosed with ALS (amyotrophic lateral sclerosis). I was heartbroken when I learned of Les’s diagnoses and the fateful experiences he would be facing. Les was the pharmacist at our facility. The fact that I worked with both of them just made it even harder to imagine that one day they would no longer be together.
At the end of 2006 I moved to Santa Monica. Les and June would sometimes visit me while Les was involved in clinical trials at UCLA. Thanks to Les’s pharmacist background, he had the foresight to do as much as possible to extend his time on earth with June. He fought ALS for seven years. I still get tears in my eyes when I think about what they both went through. I know that none of us know how long we have on this planet, but I hope we can at least try to live as much of a quality life as possible. Whether we define “quality” as spending time with loved ones, or achieving our dreams, I would love it if everyone also had optimal health as an on-going goal; because our health affects EVERYTHING!
With the recent awareness of ALS, I decided to do some research to learn more about ALS and what foods might help prevent the disease. ALS (amyotrophic lateral sclerosis), also referred to as “Lou Gehrig’s Disease,” is a progressive neurodegenerative disease that affects nerve cells in the brain and spinal cord. As these nerve cells die, they stop sending signals to body parts that allow someone to move about. Some symptoms of ALS onset include muscle weakness, noted muscle atrophy of arms or legs, difficulty with speech, swallowing or breathing.
While doing my research, I did learn that in 10% of those who get ALS, there is a family inherited genetic defect in one of the body’s own antioxidant defense systems called Copper-Zinc Superoxide Dismutase or SOD1. This type of ALS is called familial ALS or FALS. SOD1 is one of three SOD antioxidant defense systems in the body. SOD1, in particular, protects the cytoplasm, or the interior of our cells, from free-radical invaders.
Aside from FALS, the other 90% who are diagnosed with ALS, do not have an obvious genetic component. This type of ALS is termed sporadic or SALS. In all cases of ALS, it does appear that repeated oxidative damage, which occurs over time as we age, is in part, responsible for the development and progression of the disease. So, conceivably, we can prevent, or halt, or at least slow the progression of ALS by reducing or preventing oxidative damage, perhaps thwarting the efforts of oxidative invaders BY STRENGTHENING our very own antioxidant defense system. Since SOD1 a.k.a. Copper-Zinc Superoxide Dismutase, is dependent on Copper and Zinc, two essential minerals, maybe if we ensure adequate intake of these minerals through our diets, then we can help strengthen our defenses against ALS.
Upon further research, I learned of some dietary habits associated with a lower incidence of ALS. There was a study in the January 2013 issue of Annals of Neurology, which looked at the dietary habits of more than 1 million participants. Researchers found that those who ate more foods rich in colorful carotenoids, particularly from beta-carotene and lutein, had a reduced risk of developing ALS. Beta-carotene rich foods include: carrots, sweet potatoes, pumpkin, winter squash and dark leafy green vegetables. Lutein rich foods include dark leafy greens such as kale, spinach and Swiss chard, as well as collards, mustard and dandelion greens, and even green herbs such as parsley, cilantro and basil.
Another study also found that vitamin E intake was associated with reduced risk of ALS. Vitamin E is a fat soluble vitamin, which means it requires FAT to be absorbed by the body. Vitamin E is FOUND in high-fat foods: sunflower seeds are the BEST source of vitamin E, followed by almonds, hazelnuts, mixed nuts and even animal sources such as fatty fish and egg yolks. Vitamin E is often added to oils to “protect” the oil from oxidation or “breaking down.”
Because ALS has been associated with a “breakdown” in the body’s own Copper/Zinc Superoxide Dismutase antioxidant defense system (Cu/Zn SOD1), getting enough antioxidants in the diet, particularly from foods rich in beta-carotene, lutein and vitamin E, as well as copper and zinc, is especially important in the prevention of ALS.
Luckily, this recipe, like most of my recipes, happens to be rich in all of these nutrients. Although this recipe is designed with ALS prevention in mind, don’t be surprised if it also helps fight off cancer, deters the signs of aging and even reduces that menacing mid-section we see expanding with age, because a diet rich in VEGETABLES may aid weight loss.
While you’re preparing your own ALS Prevention Diet/ Recipe, please feel free to sing the following. As you sing you can ensure yourself, that you are doing this FOR YOURSELF!!!…written to Iggy Azalea’s “I’m So Fancy”
First things first I’m the healthiest. Eat this and let your whole body feel it.
‘Cause we prevent disease with the things we eat.
And I could teach you how to eat like I’m saving your life.
If you wanna be healthy like this.
Drop that soda pop and pick up a salad like this.
A quarter cup of oil, quarter cup balsamic, add water too.
A Tabelspoon Dijon, 2 cloves chopped garlic and little black pepper.
Now put it in your blender and use to top salad greens,
With a lil shredded carrot plus garbanzo beans,
Sunflower seeds and mixed nuts.
And we do it all so we can say…
I’m so Healthy, you don’t even know-o
I put greens in my…smoothies, slaws, and eggs oh, oh
I’m so healthy, can’t you see my Glow-o
I feel so vibrant and my diet makes it so-o-o-o
Eat your Veggies, they’re the things that will fight disease
Eat your veggies, and when somebody offers you greens say, “PLEASE!!”
What’s that? What’s that?
What’s that? What’s that?
What’s that? What’s that?
I’m so healthy
And my diet makes it so-o-o-o…
And I gotta go-o-o-o-o
Eat more of these FOODS!!!
Beta-carotene: Sweet potato, carrots, pumpkin, winter squash, kale, spinach
Lutein: kale, spinach, swiss chard, collards, mustard and dandelion greens
Vitamin E: sunflower seeds, almonds, hazelnuts, mixed nuts
Basic Balsamic Dijon Dressing
1/4 cup balsamic
1/4 cup extra virgin olive oil
1/4 cup water
1 Tbsp Dijon mustard
2 cloves garlic
1/4 tsp ground black pepper
ALS Prevention Salad
1 cup kale
1 cup spinach
1 shredded carrot
1/4 cup parsley
1/2 cup garbanzo beans
1 Tbsp sunflower seeds
1 Tbsp mixed nuts
Top with 2 Tbsp dressing
Cost per serving: $1.73
Nutrients per serving (10 oz-wt/ 3 1/2 cups / 296g): Calories: 360, Total Fat: 15 g, Total Carbohydrates: 42 g, Dietary Fiber: 12 g, Protein: 15 g, Sodium: 203 mg
Omega-3 Fats: 280 mg, Omega-6 fats: 5,280 mg
% Daily Value
243% vitamin A
192% vitamin C
38% vitamin E
17% riboflavin B-2
0% vitamin D
REAEARCH to accompany article:
Essays Biochem. 2014 Aug 18;56(1):149-65. doi: 10.1042/bse0560149.
Many roads lead to Rome? Multiple modes of Cu,Zn superoxide dismutase destabilization, misfolding and aggregation in amyotrophic lateral sclerosis.
Broom HR, Rumfeldt JA, Meiering EM.
ALS (amyotrophic lateral sclerosis) is a fatal neurodegenerative syndrome characterized by progressive paralysis and motor neuron death. Although the pathological mechanisms that cause ALS remain unclear, accumulating evidence supports that ALS is a protein misfolding disorder. Mutations in Cu,Zn-SOD1 (copper/zinc superoxide dismutase 1) are a common cause of familial ALS. They have complex effects on different forms of SOD1, but generally destabilize the protein and enhance various modes of misfolding and aggregation. In addition, there is some evidence that destabilized covalently modified wild-type SOD1 may be involved in disease. Among the multitude of misfolded/aggregated species observed for SOD1, multiple species may impair various cellular components at different disease stages. Newly developed antibodies that recognize different structural features of SOD1 represent a powerful tool for further unravelling the roles of different SOD1 structures in disease. Evidence for similar cellular targets of misfolded/aggregated proteins, loss of cellular proteostasis and cell-cell transmission of aggregates point to common pathological mechanisms between ALS and other misfolding diseases, such as Alzheimer’s, Parkinson’s and prion diseases, as well as serpinopathies. The recent progress in understanding the molecular basis for these devastating diseases provides numerous avenues for developing urgently needed therapeutics.
Redox Biol. 2014 Mar 26;2:632-9. doi: 10.1016/j.redox.2014.03.005. eCollection 2014.
SOD1 oxidation and formation of soluble aggregates in yeast: relevance to sporadic ALS development.
Martins D, English AM.
Misfolding and aggregation of copper-zinc superoxide dismutase (Sod1) are observed in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). Mutations in Sod1 lead to familial ALS (FALS), which is a late-onset disease. Since oxidative damage to proteins increases with age, it had been proposed that oxidation of Sod1 mutants may trigger their misfolding and aggregation in FALS. However, over 90% of ALS cases are sporadic (SALS) with no obvious genetic component. We hypothesized that oxidation could also trigger the misfolding and aggregation of wild-type Sod1 and sought to confirm this in a cellular environment. Using quiescent, stationary-phase yeast cells as a model for non-dividing motor neurons, we probed for post-translational modification (PTM) and aggregation of wild-type Sod1 extracted from these cells. By size-exclusion chromatography (SEC), we isolated two populations of Sod1 from yeast: a low-molecular weight (LMW) fraction that is catalytically active and a catalytically inactive, high-molecular weight (HMW) fraction. High-resolution mass spectrometric analysis revealed that LMW Sod1 displays no PTMs but HMW Sod1 is oxidized at Cys146 and His71, two critical residues for the stability and folding of the enzyme. HMW Sod1 is also oxidized at His120, a copper ligand, which will promote loss of this catalytic metal cofactor essential for SOD activity. Monitoring the fluorescence of a Sod1-green-fluorescent-protein fusion (Sod1-GFP) extracted
Eating bright-colored fruits and vegetables may prevent or delay ALS
New research suggests that increased consumption of foods containing colorful carotenoids, particularly beta-carotene and lutein, may prevent or delay the onset of amyotrophic lateral sclerosis (ALS). The study, published by Wiley in Annals of Neurology, a journal of the American Neurological Association and Child Neurology Society, found that diets high in lycopene, beta-cryptoxanthin, and vitamin C did not reduce ALS risk.
Carotenoids give fruits and vegetables their bright orange, red, or yellow colors, and are a source of dietary vitamin A. Prior studies report that oxidative stress plays a role in the development of ALS. Further studies have shown that individuals with high intake of antioxidants, such as vitamin E, have a reduced ALS risk. Because vitamin C or carotenoids are also antioxidants, researchers examined their relation to ALS risk.
According to the National Institutes of Neurological Disorders and Stroke (NINDS) roughly 20,000 to 30,000 Americans have ALS—also known as Lou Gehrig’s disease—and another 5,000 patients are diagnosed annually with the disease. ALS is a progressive neurological disease that attacks nerve cells (neurons) in the brain and spinal cord, which control voluntary muscles. As the upper and lower motor neurons degenerate, the muscles they control gradually weaken and waste away, leading to paralysis.
“ALS is a devastating degenerative disease that generally develops between the ages of 40 and 70, and affects more men than women,” said senior author Dr. Alberto Ascherio, Professor of Epidemiology and Nutrition at Harvard School of Public Health in Boston, Mass. “Understanding the impact of food consumption on ALS development is important. Our study is one of the largest to date to examine the role of dietary antioxidants in preventing ALS.”
Using data from five prospective groups: the National Institutes of Health (NIH)–AARP Diet and Health Study, the Cancer Prevention Study II-Nutrition Cohort, the Multiethnic Cohort, the Health Professionals Follow-up Study, and the Nurses’ Health Study, researchers investigated more than one million participants for the present study. A total of 1093 ALS cases were identified after excluding subjects with unlikely food consumption.
The team found that a greater total carotenoid intake was linked to reduced risk of ALS. Individuals who consumed more carotenoids in their diets were more likely to exercise, have an advanced degree, have higher vitamin C consumption, and take vitamin C and E supplements. Furthermore, subjects with diets high in beta-carotene and lutein—found in dark green vegetables—had a lower risk ALS risk. Researchers did not find that lycopene, beta-cryptoxanthin, and vitamin C reduced the risk of ALS. Long-term vitamin C supplement intake was also not associated with lower ALS risk.
Dr. Ascherio concludes, “Our findings suggest that consuming carotenoid-rich foods may help prevent or delay the onset of ALS. Further food-based analyses are needed to examine the impact of dietary nutrients on ALS.”
This study is published in Annals of Neurology. Media wishing to receive a PDF of this article may contact firstname.lastname@example.org
Full citation: “Intakes of Vitamin C and Carotenoids and Risk of Amyotrophic Lateral Sclerosis.” Kathryn C Fitzgerald, Eilis J O’Reilly, Elinor Fondell, Guido J Falcone, Marjorie L McCullough, Yikyung Park, Laurence N Kolonel and Alberto Ascherio. Annals of Neurology; Published Online: January 29, 2013 (DOI:10.1002/ana.23820).
Author Contact: To arrange an interview with Dr. Ascherio, please contact Todd Datz with the Harvard School of Public Health at email@example.com.
About the Journal
Annals of Neurology, the official journal of the American Neurological Association and the Child Neurology Society, publishes articles of broad interest with potential for high impact in understanding the mechanisms and treatment of diseases of the human nervous system. All areas of clinical and basic neuroscience, including new technologies, cellular and molecular neurobiology, population sciences, and studies of behavior, addiction, and psychiatric diseases are of interest to the journal. The journal is published by Wiley on behalf of the American Neurological Association and Child Neurology Society. For more information, please visit http://onlinelibrary.wiley.com/journal/10.1002/ana.
Metabolism. 2000 Feb;49(2 Suppl 1):3-8.
What is oxidative stress?
Oxidative stress, defined as a disturbance in the balance between the production of reactive oxygen species (free radicals) and antioxidant defenses, is discussed in relation to its possible role in the production of tissue damage in diabetes mellitus. Important free radicals are described and biological sources of origin discussed, together with the major antioxidant defense mechanisms. Examples of the possible consequences of free radical damage are provided with special emphasis on lipid peroxidation. Finally, the question of whether oxidative stress is increased in diabetes mellitus is discussed.
Weight loss effects from vegetable intake: a 12-month randomised controlled trial.
Direct evidence for the effects of vegetable intake on weight loss is qualified. The study aimed to assess the effect of higher vegetable consumption on weight loss.
A single blind parallel controlled trial was conducted with 120 overweight adults (mean body mass index=29.98 kg/m(2)) randomised to two energy deficit healthy diet advice groups differing only by doubling the serving (portion) sizes of vegetables in the comparator group. Data were analysed as intention-to-treat using a linear mixed model. Spearmans rho bivariate was used to explore relationships between percentage energy from vegetables and weight loss.
After 12 months, the study sample lost 6.5±5.2 kg (P<0.001 time) with no difference between groups (P>0.05 interaction). Both groups increased vegetable intake and lost weight in the first 3 months, and the change in weight was significantly correlated with higher proportions of energy consumed as vegetables (rho=-0.217, P=0.024). Fasting glucose, insulin and triglyceride levels decreased (P<0.001 time) and high-density lipoprotein cholesterol levels increased (P<0.001 time), with no difference between groups. Weight loss was sustained for 12 months by both groups, but the comparator group reported greater hunger satisfaction (P=0.005).
Advice to consume a healthy low-energy diet leads to sustained weight loss, with reductions in cardiovascular disease risk factors regardless of an emphasis on more vegetables. In the short term, consuming a higher proportion of the dietary energy as vegetables may support a greater weight loss and the dietary pattern appears sustainable.