
Today, one of every seven
Americans will experience movement disorders. Movement
disorders
encompass a number of debilitating conditions including
Parkinson’s Disease,
dystonia, torticollis, hemifacial spasm, tremors, and many other
involuntary movements or muscle
spasm from conditions like MS, stroke and cerebral palsy. Often
symptoms
do not manifest until later in life, and are growing in occurrence.
The most common treatments
pursued by doctors typically depend on oral medications. While
sometimes successful in reducing
motor symptoms, the effects of medications
vary from person to person. Some drugs may be ineffective on certain
individuals, and many trigger serious or disabling side effects.
Experimenting with medications and treating corollary
ailments can result in medical bills that add up into the thousands
each month. Furthermore, in advanced cases, and even some mild cases,
side effects resulting from medications may be more severe than the
symptoms being treated.
NSC offers innovative
medications, nerve blocks and effective surgical options for better
muscular control and improved quality of life. These advanced
interventions offer patients a significant reduction in
oral medications, relief from behavioral and cognitive side effects,
and more effective motion control, which is essential for the
successful treatment of movement disorders. As the first sub-specialty
movement disorder clinic of its kind in central Texas, NSC also
provides
general neurologists and primary care physicians access to the latest
services
and treatments available today.
DEEP
BRAIN STIMULATION
Excerpt from NINDS
(National Institute of Neurological Disorders and Stroke) NIH
Deep brain stimulation
(DBS) is a surgical procedure used to treat a variety of disabling
neurological symptoms—most commonly the debilitating symptoms
of Parkinson’s disease (PD), such as tremor, rigidity,
stiffness, slowed movement, and walking problems. The
procedure is also used to treat essential tremor, a common neurological
movement disorder. At present, the procedure is used only for
patients whose symptoms cannot be adequately controlled with
medications.
DBS uses a surgically
implanted, battery-operated medical device called a
neurostimulator—similar to a heart pacemaker and
approximately the size of a stopwatch—to deliver electrical
stimulation to targeted areas in the brain that control movement,
blocking the abnormal nerve signals that cause tremor and PD symptoms.
Before the procedure, a
neurosurgeon uses magnetic resonance imaging (MRI) or computed
tomography (CT) scanning to identify and locate the exact target within
the brain where electrical nerve signals generate the PD
symptoms. Some surgeons may use microelectrode
recording—which involves a small wire that monitors the
activity of nerve cells in the target area—to more
specifically identify the precise brain target that will be
stimulated. Generally, these targets are the thalamus,
subthalamic nucleus, and globus pallidus.
The DBS system consists of
three components: the lead, the extension, and the
neurostimulator. The lead (also called an
electrode)—a thin, insulated wire—is inserted
through a small opening in the skull and implanted in the
brain. The tip of the electrode is positioned within the
targeted brain area.
The extension is an
insulated wire that is passed under the skin of the head, neck, and
shoulder, connectng the lead to the neurostimulator. The
neurostimulator (the "battery pack") is the third component and is
usually implanted under the skin near the collarbone. In some
cases it may be implanted lower in the chest or under the skin over the
abdomen.
Once the system is in
place, electrical impulses are sent from the neurostimulator up along
the extension wire and the lead and into the brain. These
impulses interfere with and block the electrical signals that cause PD
symptoms.
Select this link to view a list of
studies currently seeking patients.
Prepared by:
Office of
Communications and Public Liaison
National Institute of Neurological Disorders and Stroke
National Institutes of Health
Bethesda, MD 20892
BACLOFEN PUMP THERAPY
Baclofen acts by
stimulating GABA type B receptors in the spinal cord and oral baclofen
is often helpful in the treatment of spasticity. In order to avoid the
side effects of high oral doses of baclofen, the medicine may be
continuously administered into the space surrounding the spinal cord
via a pump. The pump is implanted in the abdomen and connected to a
small tube. This tube is tunneled under the skin around the back and
then inserted into the space around the spinal cord (the intrathecal
space). Very small doses are given. The pump is refilled approximately
every three months by injection directly through the skin into the
pump's reservoir. This technique is extremely effective for some
children with spasticity or dystonia that affects the arms and legs. If
it is not effective, the pump and tubing may be removed without
significant permanent effects. This therapy is associated with
complications including pump infections, catheter problems, and spinal
fluid leakage around the catheter into the subcutaneous tissues.
Baclofen withdrawal is another potential complication. In spite of the
complications, the majority of patients and families who are treated
with ITB feel that the benefits of treatment outweigh the risks. Recent
reports suggest that the baclofen pump may also be helpful in
generalized dystonia, although the mechanism of this effect is not
known.
Intrathecal
Pump Story from University of Texas at Houston Medical School
BOTULINUM
TOXIN THERAPY
BOTOX® is
indicated for the treatment of cervical dystonia in adults to decrease
the severity of abnormal head position and neck pain associated with
cervical dystonia. Cervical dystonia (CD), also known as spasmodic
torticollis, belongs to a group of disorders known as focal dystonias.
These disorders are characterized by involuntary tonic contractions or
intermittent spasms of the neck muscles, causing rotational
(torticollis), lateral (laterocollis), forward (anterocollis), or
backward (retrocollis) tilting of the head.1
CD is often associated
with a high incidence of pain. In fact, one study showed that more than
90% of patients with CD experience pain.2
CD occurs in 9 out of
every 100,000 individuals.3 Approximately 5% to 16% of patients with CD
have a history of head or neck trauma preceding the onset of dystonia.4
The true cause of CD, however, is unknown at this time.
The defining feature in
dystonias is sustained muscle contractions leading to repetitive
twisting movements and abnormal postures. Although onset may occur at
any age, it typically occurs in adults between the ages of 30 and 70.
Women are nearly twice as likely to be affected with CD as men.2
Symptoms usually appear
gradually though an acute onset is not uncommon. Patients usually
present with painful, tonic contractions or intermittent spasms of the
sternocleidomastoid, trapezius, or other neck muscles that are limited
to one side of their body. These contractions force the head into
abnormal positions.
The pain associated with
CD is usually rated as moderate to severe. In severe cases, the
disorder may impair a patient's ability to move or may lead to postural
deformity. Generalized and focal forms of dystonia usually stabilize
within 5 years of onset; however, symptoms may fluctuate, particularly
during times of stress. Generally, late-onset dystonia usually
progresses to a certain point then plateaus.5
A small percentage of CD
patients (approximately 10% to 20%) may experience remission within 5
years of onset. Approximately 33% of CD patients show evidence of
dystonia elsewhere on the body, such as the eyelids, face, jaw, or
hand. Active spasms (ie, involuntary movements) disappear during sleep.6
BOTOX® (Botulinum
Toxin Type A) Purified Neurotoxin Complex blocks the nerve impulses
that trigger muscle hyperactivity. Although the exact mechanism of
action is not yet known, the neurotoxin is thought to bind to certain
receptors on cholinergic terminals on nerve endings. The neurotoxin is
then absorbed into the nerve ending, where it interferes with the
cholinergic vesicles that release acetylcholine. This interference
leads to chemodenervation and reduced muscular contractions.7
In 2000, the FDA approved
BOTOX® for the treatment of CD in adults to decrease the
severity of abnormal head position and neck pain associated with CD.7
Each BOTOX®
treatment lasts up to three months. Patients eventually return to
pretreatment status at which point they can be reinjected over time
with the neurotoxin as long as they continue to respond and do not have
a serious allergic reaction.7
Patients with
neuromuscular disorders may be at increased risk of clinically
significant systemic effects including severe dysphagia and respiratory
compromise from typical doses of BOTOX®. The effects of therapy
may be increased with the use of aminoglycoside antibiotics or with
other drugs that interfere with neuromuscular transmission.
There have been rare
spontaneous reports of death, sometimes associated with dysphagia,
pneumonia, and/or other significant debility or anaphylaxis, after
treatment with botulinum toxin. Patients with smaller neck muscle mass
and patients who require bilateral injections into the
sternocleidomastoid muscle have been reported to be at greater risk for
dysphagia. Limiting the dose injected into the sternocleidomastoid
muscle may reduce the occurrence of dysphagia. Injections into the
levator scapulae may be associated with an increased risk of upper
respiratory infection and dysphagia.
| 1 |
Fahn S,
Marsden CD, Calne DB. Classification and investigation of dystonia. Mov
Disord. 1987;2:332-358. |
| 2 |
Chan J,
Brin MF, Fahn S. Idiopathic cervical dystonia: clinical
characteristics. Mov Disord. 1991;6:119-126. |
| 3 |
Data on
File, Allergan, Inc. |
| 4 |
Van
Zandijcke M. Cervical dystonia (spasmodic torticollis). Some aspects of
the natural history. Acta Neurol Belg. 1995;95(4):210-215. |
| 5 |
Dystonia
Medical Research Foundation. Available at: http://www.dystonia-foundation.org/.
Accessed January 12, 2001. |
| 6 |
Merck Manual.
Available at: http://www.merck.com/pubs/mmanual/section5/chapter59/59a.htm
Accessed January 12, 2001.
|
| 7 |
BOTOX®
Full Prescribing Information. |
Blepharospasm is a
localized movement disorder (focal dystonia) that affects the muscles
that control eyelid movement. The disorder is characterized by
increased blinking caused by involuntary spasms of the muscles
controlling the eyelid. Blepharospasm usually affects both eyelids and
can progress to functional blindness (ie, an inability to open the
eyelids for any significant period of time).
Approximately 75% of
patients with blepharospasm are female and the average age at onset is
56 years.1 Although the exact cause of this disorder is unknown,
experts believe that it may be caused by a defect in the basal
ganglia–a group of nerve cells in the central nervous system.2
BOTOX® injected
directly in the affected eye muscles relieves the muscle spasm within
48 hours. The duration of effect lasts up to three months at which time
the neurotoxin can be reinjected as long as the patient continues to
respond and does not have a serious allergic
reaction.3
| 1 |
Henderson
JW. Essential blepharospasm. Trans Am Ophthalmol Soc. 1956;54:453-520. |
| 2 |
Dystonia
Medical Research Foundation. Available at: http://www.dystonia-foundation.org/.
Accessed January 12, 2001. |
| 3 |
BOTOX®
Full Prescribing Information. |
|
ANTIINFLAMMATORY AND ANTIOXIDANT STRATAGIES
Brain Defense Supplements
by Rob Izor, MD, MS
April 12, 2008
Supplements
or “nutraceuticals” and other “alternative
medicine” approaches have potential to significantly influence
our health, sometimes for the better. However, some approaches may
cause unintended side effects and even irreversible damage. The goal of
this brief summary is to explain the basis for certain antioxidant and
anti-inflammatory strategies for neurodegenerative disease,
particularly Parkinson's Disease.
Because
“food supplements” do not undergo FDA testing for safety
and efficacy, the benefits and risks of any given supplement or brand
of supplement are much less certain than with regulated prescription
medications. On the other hand, prescription medications may also have
unintended dangers that do not surface until many have been injured,
sometimes irreversibly. A good example is the prescription pain
medication Vioxx, which increased risk for strokes and heart attacks.
Prescription drug makers have legal requirements which motivate them to
report severe side effects or complications to the FDA. This sometimes
helps identify problems early so recalls can be implemented before more
people are injured. Supplements do not have these reporting
requirements, and therefore serious complications are not necessarily
identified or reported. As with prescription medications, patients and
doctors must weigh risks and benefits before proceeding with any
treatment plan. Weighing risks can be more difficult with nutritional
supplements and non-FDA approved uses of prescription medications.
Research
over the last several years indicates neuroinflammation and free
radical oxidative stress play major roles in the propagation, if not
underlying cause, of neurodegenerative diseases. There are
multifactorial genetic, environmental, and age related processes which
may promote loss of brain function. However, the presence of
inflammation adds fuel to the fire. A genetic study implicates two
inflammatory local hormones (cytokines); TNFa and IL-1b increase the
risk for Parkinson's Disease1. Recent experiments in patients using a
drug that blocks TNFa (etanercept) has shown remarkable improvement in
cognitive function in advanced Alzheimer's disease (AD). AD is another
neurodegenerative disease in which neuroinflammation plays a major
role.2 Oxidizing free radical byproducts of metabolism have also been
implicated, triggering production of potentially damaging inflammatory
cytokines.3
Antioxidant
and anti-inflammatory nutritional supplements may have a preventive
role by modifying cytokines and associated signals which lead to
programmed cell death (apoptosis). A few supplements in particular have
been found to mitigate damage caused by oxidative stress and/or reduce
the activity of TNFa and other inflammatory cytokine pathways. These
supplements include B12, Folate, N-acetyl-L-cysteine, alpha lipoic
acid, and DHA (omega-3) fatty acids. Dextromethorphan and the
prescription drug naltrexone (non-FDA approved use) also have important
anti-inflammatory and potentially neuroprotective properties which
should be considered.
B12/Folate/B6/Homocysteine
Vitamins
B12, B6 and folate are metabolic cofactors important for cellular
metabolism and maintenance of all tissue cell types, but particularly
important to nerve cells. B12 is found in animal products, meats, and
fish. Folate is found in green vegetables. B6 is present in whole grain
foods and animal products. B12 absorption from the intestine is a
complicated process and tends to diminish with age. Several metabolic
disturbances are known to deplete B12. B12 deficiency can damage the
nervous system leading to neuropathy, myelopathy, and dementia.
Furthermore, B12, B6, and folate work together to regulate homocysteine
levels. Deficiencies in B12 or folate can raise homocysteine levels.
Elevated homocysteine levels have been associated with a higher risk
for vascular disease, dementia, and directly or indirectly increases in
oxidative stress. The role in neurodegenerative disease is unclear, but
elevated homocysteine has been associated with PD and may aggravate the
neurodegenerative process.4
B12
deficiency is typically diagnosed by blood tests. However, one study in
Alzheimer's patients demonstrated normal blood levels, when in fact
cerebrospinal fluid levels were low compared to control subjects.5
Testing blood B12 levels is probably not a good indicator of the true
B12 status in the central nervous system. B12 and folate
supplementation has not been adequately studied in Parkinson's Disease;
however, due to potentially shared mechanisms in neurodegeneration,
active supplementation of B12, folate, and other antioxidants may be
beneficial in promoting better neurological health.
N-acetyl-L-cysteine (NAC)
NAC is
a precursor to glutathione, the body’s most important cellular
antioxidant. NAC supplementation has been shown to increase cellular
glutathione levels. NAC relieves oxidative stress, reduces the
apoptotic effects of TNFa, and has many other documented benefits.
Glutathione function diminishes with aging and is particularly reduced
in neurodegenerative states. In Parkinson's research, NAC has been
shown to reduce MPTP toxin induced TNFa and associated apoptosis
in mice.6 Early studies in Alzheimer's disease indicate
improvement in cognitive scores after 6 months treatment.7 Human
studies in Parkinson's Disease are lacking at this time.
Alpha Lipoic Acid (ALA)
ALA is
an essential cofactor in normal cellular metabolism and cellular energy
production. ALA is also an antioxidant free radical scavenger and heavy
metal chelator. ALA has the capability of regenerating the antioxidant
function of glutathione, vitamin C, and vitamin E and can reverse
symptoms caused by vitamin C and E deficiencies. The use of ALA as a
supplement is under investigation, and has demonstrated improvements in
peripheral neuropathy8, Alzheimer's disease9, and insulin resistant
type II diabetes10. Several studies indicate ALA inhibits TNFa induced
apoptosis which may support a neuroprotective effect11. ALA has not yet
been studied in Parkinson's disease in humans; however, MPTP toxic
animal models of PD have shown evidence of neuroprotection from MPTP12.
There are two forms of ALA, called R and S enantiomers. The R version
is considered the more active form. Most supplements are a 50/50
mixture of R/S.
Opioid Antagonists (Dextromethorphan and low dose naltrexone (LDN))
Naltrexone
is actually a prescription drug, but can be compounded into a lower
dose form, LDN, which imparts significant indirect anti-inflammatory
properties. Dextromethorphan may also have similar properties and is
available over-the-counter as a cough suppressant. LDN shows
promising results in early studies of MS and Crohn’s Disease,
both characterized by abnormal inflammation. Effects on the
endogenous opioid system (endorphins, enkephalins) inhibit many
inflammatory mediators, including TNFa and IL-6. A few studies support
a potential neuroprotective effect of LDN and dextromethorphan.13, 14,
15 The mechanism whereby LDN or dextromethorphan reduces inflammation
is thought related to modulation of endorphin receptors and related
immunomodulatory effects.16 Opiod receptors have also been implicated
as important modulators of neurotrophic growth factors, GDNF and
BDNF.17
Use of
antioxidant supplements and/or low dose opioid antagonists may have
important neuroprotective and anti-inflammatory effects which might
benefit PD and other neurodegenerative and inflammatory conditions. All
these supplements should be considered drugs and only used only under
the supervision of a physician. More research is needed before any can
be safely recommended as an effective treatment for any
neurodegenerative disease. Until such research becomes available, I
believe patients should be made aware of these potential benefits and
proceed cautiously in choosing to take these drugs as an adjunct to
standard medical treatments. So far, data does not support significant
short term risks at dosing ranges used in human studies. However, long
term daily usage may surprise us with unknown and unpredictable
complications. Therefore risks, both known and unknown, must be weighed
carefully with the potential benefits. Unfortunately, standard
treatments for most neurodegenerative diseases like PD confer little if
any neuroprotective benefit, which makes alternative strategies very
attractive in spite of limited data supporting efficacy.
.
- Wahner AD,
et.al. Inflammatory cytokine gene polymorphisms and increased risk
of Parkinson disease. Arch Neurol 01-JUN-2007; 64(6): 836-40
- Tobinick E,
et.al. Perispinal etanercept for treatment of Alzheimer's disease.
Curr Alzheimer Res 01-DEC-2007; 4(5): 550-2
- Shibata N,
et.al. The role for oxidative stress in neurodegenerative diseases.
Brain Nerve 01-FEB-2008; 60(2): 157-70
- Obeid R, et.al.
Mechanisms of homocysteine neurotoxicity in neurodegenerative
diseases with special reference to dementia. FEBS Lett 29-MAY-2006;
580(13): 2994-3005
- Regland B,
et.al. Vitamin B12 in CSF: reduced CSF/serum B12 ratio in demented
men. Acta Neurol Scand 01-APR-1992; 85(4): 276-81
- Chen CM, et.al.
Antioxidative and anti-inflammatory effects of four
cysteine-containing agents in striatum of MPTP-treated mice.
Nutrition 01-JUL-2007; 23(7-8): 589-97
- Adair JC, Knoefel JE, Morgan N.
Controlled trial of N-acetylcysteine for patients with probable
Alzheimer's disease. Neurology. 2001 Oct 23;57(8):1515-7
- Ametov AS, et.al. The sensory symptoms
of diabetic polyneuropathy are improved with alpha-lipoic acid: the
SYDNEY trial. Diabetes Care. 2003 Mar;26(3):770-6
- Hager K, Kenklies M, McAfoose J, Engel
J, Münch G. Alpha-lipoic acid as a new treatment option for
Alzheimer's disease--a 48 months follow-up analysis. J Neural Transm
Suppl. 2007;(72):189-93
- Jacob S, et al.
Enhancement of glucose disposal in patients with type 2 diabetes
mellitus by alpha-lipoic acid. Arzneimittelforschung 1995; 45:872—4
- Byun
CH, et.al. Alpha-lipoic acid inhibits TNF-alpha-induced apoptosis in
human bone marrow stromal cells. J Bone Miner Res. 2005
Jul;20(7):1125-35
- Karunakaran
S, et.al. Activation of apoptosis signal regulating kinase 1 (ASK1)
and translocation of death-associated protein, Daxx, in substantia
nigra pars compacta in a mouse model of Parkinson's disease:
protection by alpha-lipoic acid. FASEB J. 2007 Jul;21(9):2226-36
- Qin
L, et.al. Microglial NADPH oxidase is a novel target for femtomolar
neuroprotection against oxidative stress. FASEB J. 2005
Apr;19(6):550-7
- Li G, et.al. Femtomolar concentrations
of dextromethorphan protect mesencephalic dopaminergic neurons from
inflammatory damage. FASEB J. 2005 Apr;19(6):489-96
- Zhang W, Wang T, Qin L, Gao HM, Wilson
B, Ali SF, Zhang W, Hong JS, Liu B. Neuroprotective effect of
dextromethorphan in the MPTP Parkinson's disease model: role of NADPH
oxidase. FASEB J. 2004 Mar;18(3):589-91. Epub 2004 Jan 20
- Tegeder I, Geisslinger G. Opioids as
modulators of cell death and survival--unraveling mechanisms and
revealing new indications. Pharmacol Rev. 2004 Sep;56(3):351-69
- Narita M, et.al. Role of delta-opioid
receptor function in neurogenesis and neuroprotection. J Neurochem.
2006 Jun;97(5):1494-505
CURRENT SOURCES AND PRICES OF SUPPLEMENTS RECOMMENDED BY DR. IZOR
(do not take any supplements without
reviewing with your physician, and obtaining written instructions on
dosages and side effects)
THE BRAIN DEFENSE DIET
by Rob Izor MD, MS
January 1, 2007
Scientific
literature outlines serious health risks caused by diets containing
processed “trans” unsaturated fat, high saturated fat and
high omega 6 fat. Replacing these bad fats with foods containing a
better ratio of monounsaturated and natural “cis”
unsaturated fats will significantly reduce risk for heart disease,
stroke and many chronic diseases like Parkinson's and dementia. Until
the general population demands healthy fast foods and restaurant
ingredients, we will need to take individual responsibility for our
health, and spend the time and resources necessary to insure a healthy
diet. My goal with this brief summary is to give you my best current
opinion regarding dietary recommendations after reviewing and compiling
readily available literature on this subject. There are still
controversies about best recommendations, complicated by many myths.
But choosing an active, vital role in your dietary health is in your
best interest. Eating processed food blindly is dangerous to your long
term health and will likely accelerate disability from chronic disease.
Food
suppliers have been forced by the FDA to expand labeling of fat
content, and to at least partly recognize the dangers of certain
fats. “Trans” unsaturated fat, also called partially
hydrogenated fat, intentionally created during commercial food
processing for fat stabilization, has now been linked to heart disease,
stroke and contributes to many other health risks. Some food companies
are reducing or eliminating “trans” fats. However, labeling
flexibility from the FDA allows many foods to be labeled as 0 grams
“trans” fats per serving, but actually contain up to 0.5
grams per serving. This could still add up to significant exposure with
multiple servings per day. There are other dangerous ingredients
present in commercially processed and refined foods which should be
avoided for the most part. Healthier, unrefined foods with good fats
tend to cost more for ingredients and preparation, and are therefore
less available in restaurants, if at all.
Our
fast food western diet is typically high in saturated fats and simple
carbohydrates like starch and enriched wheat. Polyunsaturated omega 6
to omega 3 fat ratios are as high as 40:1 (heavily lopsided toward
omega 6 with very little or no omega 3 fat.) Large amounts of saturated
fats are physiologically destructive, and should be minimized.
Replacing saturated fats with monounsaturated and polyunsaturated fats
lowers LDL cholesterol, raises healthy HDL cholesterol, and is
protective for your health. Higher omega 3 fat intake is protective,
and too much omega 6 increases health risks. Ratios of these fat
subtypes vary widely in different foods which makes choosing the right
combination of food ingredients even more complex. A simplistic answer
to avoid the dangers of certain fats might be to seek a “low
fat” diet, even substituting natural foods with processed, low
fat food substitutes and/or health shakes or bars. However, avoiding
good fat (favorable omega 3:6 ratios, and monounsaturated omega 9 fats)
is also unhealthy, and most food substitutes are too low in the good
fats.
In retrospect, low fat diets generally favor consumption of higher
calorie, less filling, refined carbohydrates which also increase bad
“LDL” cholesterol and triglycerides. Eventually, high
LDL cholesterol, high triglycerides and high simple carbohydrates are
associated with obesity, diabetes, hypertension and reduced
circulation. These risk factors lead to vascular disease, heart
attacks, strokes and dementia. Stroke and heart disease are the leading
causes of death, and stroke is the leading cause of disability in the
United States. These same dietary risks increase risk for vascular and
Alzheimer's dementia, Parkinson's disease, and perhaps other
neurodegenerative diseases which are also important causes of
disability.
EATING
a balance of GOOD FATS, protein and complex carbohydrates (whole grain,
unrefined foods,) while AVOIDING BAD FATS (saturated and high ratio
omega 6 fats) and limiting REFINED CARBOHYDRATES, STARCHES AND SUGARS
may be the best way to maintain better health. Reducing saturated fats
and simple carbohydrates, starches and refined sugars may also be
important in reducing overall inflammation and supporting better immune
function. Eating or supplementing more omega 3 may help offset health
risks caused by too much omega 6. Therefore whenever possible, try to
avoid, reduce and/or replace foods rich in saturated fat and omega 6
fat, with foods richer in omega 3 and monounsaturated fats (omega 9.)
Aim to achieve a ratio of 1:1 omega 6 to omega 3 over the day. A 4:1
ratio has been suggested as adequate for good health, but foods with
more omega 3 and less omega 6 fats are probably even better. So on
average, for every one (to four) gram(s) of omega 6 in your diet, you
should strive to eat foods which include at least one gram of omega 3.
Supplementing your diet with omega 3 rich flaxseed oil and/or EPA/DHA
fish oil supplements may also be a helpful strategy. The following AHA
guidelines are reasonable targets for total fat intake and cholesterol.
As previously outlined, eating foods with up to 0.5 grams of trans fat
(which are labeled 0 grams) could easily overwhelm these
recommendations if several servings add up over the day. Therefore,
carefully look at the ingredients and avoid foods with any partially
hydrogenated fats.
“The
American Heart Association's Nutrition Committee strongly advises these
fat guidelines for healthy Americans over age 2:
Limit total fat intake to less than 25–35 percent of your total calories each day;
Limit saturated fat intake to less than 7 percent of total daily calories;
Limit trans fat intake to less than 1 percent of total daily calories;
The
remaining fat should come from sources of monounsaturated and
polyunsaturated fats such as nuts, seeds, fish and vegetable oils; and
Limit
cholesterol intake to less than 300 mg per day, for most people.
If you have coronary heart disease or your LDL cholesterol level is 100
mg/dL or greater, limit your cholesterol intake to less than 200
milligrams a day.
For
example, a sedentary female who is 31–50 years old needs about
2,000 calories each day. Therefore, she should consume less than 16 g
saturated fat, less than 2 g trans fat, and between 50 and 70 grams of
total fat each day (with most fats coming from sources of
polyunsaturated and monounsaturated fats, such as fish, nuts, seeds and
vegetable oils).”
9 Steps for a Brain Defense Diet:
1.Eat
more fish, beans, vegetables, nuts, fruits, and juices. Avoid farmed
fish. Avoid foods or juices with added refined sugar or corn syrup.
Consider diluting fruit juices and vegetable juices with 50% purified
water to reduce total calories.
2.Avoid
red meats from sedentary farm animals (high saturated fats, high omega
6.) Choose organic, free range, grass or flaxseed fed meats which have
better omega 3 ratios and less saturated fat. Low fat cuts of game
meats like venison are good too. Trim all excess fat before cooking.
3.Eat
whole grain breads, brown rice and whole grain pastas while avoiding
simple carbohydrates, starches and refined sugars. Limit white
potatoes, french fries, white breads, white tortillas, white rolls,
enriched pastas, white rice, refined corn products, and anything that
has enriched wheat, starch or dextrose as a main ingredient.
4.Avoid
foods and oils high in saturated fat (more than 10% of total fat.)
Avoid foods with hydrogenated or partially hydrogenated oil listed in
the ingredients, even if label states 0 grams “trans” fat.
Use organic macadamia nut oil or canola oil for cooking or frying.
Canola is low in saturated and omega 6 fats, and high in omega 3. Olive
oil is higher in omega 6 and low in omega 3. Do not overheat oils,
especially olive oil. If you see smoke, its too late. Buy cold pressed
oils in small quantities (extra virgin olive oil) and replace every few
months. Flaxseed oil cannot be heated and must be refrigerated. These
types of oils are more expensive to produce. Better oil is expensive,
so consider using smaller amounts when cooking or frying to help offset
the cost.
5.Add
ground flaxseeds, 1-2 tbs to whole grain cereal or oatmeal for
breakfast using fat free skim milk. If too bitter, use a ½ tbs
of cold pressed flaxseed oil instead.
6.Avoid regular egg yolks. Instead choose free range, flaxseed fed chicken eggs.
7.Limit foods or spreads with large amounts of saturated and omega 6 fats; (corn, safflower, soybean or other vegetable oils.)
8.Avoid
foods with MSG (monosodium glutamate) and other preservatives
“taste enhancers” (glutamic acid, amino acid derivatives.)
9.Use EPA/DHA omega 3 nutritional supplements low in omega 6.
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