Dauntless
100 TW

You win It's hopeless.

Get some medical help. Good place to start is a primary doctor.
C4 helps control the shoulders as well as the diaphragm—the sheet of muscle that stretches to the bottom of the rib cage—for breathing. The C4 dermatome covers the neck and top of the shoulders.
"Cut C4, breathe no more."
Interestingly, the C4 nerve also supplies the anterior chest wall to the nipple line. Compression of this nerve can sometimes mimic chest pain from a heart attack (called cervical angina).
C1, C2, and C3 (the first three cervical nerves) control the head and neck, including movements forward, backward, and to the sides. These nerves also play key roles in breathing. The C2 dermatome handles sensation for the upper part of the head, and the C3 dermatome covers the side of the face and behind the head. (C1 does not have a dermatome.)
Compression of these nerve roots can cause neck pain but generally do not connect to any muscles. Injury to these nerves will therefore not cause arm weakness. Even within this group, the first two nerves (C1 and C2) are different as these two nerves (AKA the greater and lesser occipital nerves) supply sensation to the back of the skull and irritation can generate headaches. The C3 and C4 nerves supply sensation to the neck and very top of the shoulders. Numbness, paresthesias (pins and needles) and pain will follow the distribution of these nerves.
Unilateral diaphragmatic paralysis or weakness rarely causes symptomatic dyspnea at rest, but may result in dyspnea on exertion or the patient's voluntary restriction of activity. It can sometimes cause dyspnea when lying on one's back (supine). Often, unilateral diaphragmatic paralysis is detected incidentally on a chest X-ray obtained for other purposes.
Bilateral diaphragmatic paralysis frequently causes dyspnea at rest, with exertion, when supine (necessitating sleeping in a recliner), bending over, or when swimming with water above waist level. Sleep disorders are also common in these patients, and symptoms thereof (fatigue, somnolence, awakening during sleep) may be the first presentation of bilateral diaphragmatic paralysis. Recurrent pneumonias (possibly due to basilar atelectasis) and recurrent respiratory failure are also possible.
To estimate this decrease, take your pulse one minute after you finish running. Subtract this number from the highest heart rate you achieved while running. A difference of less than 12 beats per minute, or bpm, may indicate poor cardiovascular health.
By 10 minutes after exercise, though, your heart rate should be below 100 bpm
By 30 minutes after exercise, your heart rate should return to normal, say health advisers for the Federal Aviation Administration. If your heart rate remains higher than 100 bpm for 30 minutes or longer after running, consult a medical professional
Swbluto's still with us. This post:Dauntless said:Almost a day and a half with no symptoms posted. Think he checked out?
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nutspecial said:Uhhh, wtf that isn't some digital demonic activity though, I hope?
(was just watching 'friend request' 2016)![]()
http://fitness.stackexchange.com/questions/2163/tingling-in-fingertips-and-lips-on-a-hard-run
Yes, you are experiencing a lack of blood flow, and thus oxygen deprivation, to those parts of your body. Most of your blood will be pumping through your legs (actually, your legs are helping to push blood through your heart) and less will be flowing to other areas of the body, specifically areas level with or above the heart will take the largest deficit of blood flow and oxygen. If you are experiencing a tingling sensation like that, then you need to slow down and let your body regain some oxygen.
If you are running with your arms out, or your elbows bent at greater than a 90 degree angle, you are more likely to experience the tingling in your fingers. Your hands will likely be raised higher than your heart, and an increased bend in your elbow will also create a tighter area for the blood to pump through. You can't really lower your head below your heart when you're running though, and your brain is in your head, so if you are experiencing a lack of oxygen to your fingers and lips, you are also experiencing a lack of oxygen to your brain, and this can cause damage or in extreme cases even be fatal.
Panic attacks may be accompanied by sharp and abrupt chest pain, most likely caused by muscle contractions in the chest wall. The chest wall may feel sore for hours or days after a panic attack.
As many patients who sustain navicular stress fractures are athletes, they initially may complain of pain only during sport and not with other activities of daily living.8,10 Specifically, explosive activities such as jumping, sprinting and rapidly changing direction may exacerbate symptoms.
A diastolic blood pressure of somewhere between 90 and 60 is good in older folks. Once you start getting below 60, that makes people feel uncomfortable. A lot of older folks with low diastolic pressures get tired or dizzy and have frequent falls. Obviously, none of that is good news for people who are older, who potentially have brittle bones and other issues.
MayoClinic.com says that low blood pressure can be caused by a number of heart problems or defects. A low heart rate, also known as bradycardia, can cause a drop in blood pressure. Diastolic pressure can also be affected by heart valve problems, a heart attack or heart failure. In these situations, the heart cannot circulate the amount of blood that is needed.
MedlinePlus warns that dehydration can cause a drop in blood pressure. When the body is dehydrated, the blood volume drops, which can lead to a marked drop in diastolic blood pressure.
A severe lack of certain nutrients, such as vitamin B-12 or folate, has been known to cause anemia. This condition means your body does not produce an adequate number of red blood cells and low blood pressure results, according to MayoClinic.com.
http://nutritiondata.self.com/foods-002112000000000000000-w.html?maxCount=25
However, if the pain is severe or you are uncertain about its cause, consult your physician immediately.
Blood pressure, mm Hg
Systolic
126.7 ± 15.9
136.5 ± 19.3
135.1 ± 19.3
Diastolic
80.9 ± 10.5
81.5 ± 11.2
75.2 ± 11.1
Prepare a mixture using the herb Indian spikenard. Steep 15 to 20g of Indian spikenard in boiling water. Add a pinch of camphor and cinnamon, and drink a cup three times a day to raise your diastolic pressure.
Spikenard, also called nard, nardin, and muskroot, is a class of aromatic amber-colored essential oil derived from Nardostachys jatamansi, a flowering plant of the Valerian family which grows in the Himalayas of Nepal, China, and India.
a sedative, and an herbal medicine said to fight insomnia
The Kuna have been shown to have a low average blood pressure (BP, 110/70 mm Hg)
VBI, often provoked by sudden and temporary drops in blood pressure, can cause transient ischemic attacks. Postural changes (see orthostatic hypotension), such as getting out of bed too quickly or standing up after sitting for extended periods of time, often provoke these attacks
Mechanical forces acting upon the neck at any age can cause VBI by exacerbating arterial insufficiency or outright occluding one or both vertebrobasilar arteries. Internal forces include those caused by turning the head to an extreme angle to the side, especially with the neck extended. The patient can create this condition while driving a vehicle in reverse, shooting a bow and arrow, bird watching, or stargazing.
If you are prone to dizzy spells, you should avoid any over-the-counter medications that cite dizziness as a possible side effect, such as antihistamines or sleeping aids. Caffeine, tobacco and alcohol can also intensify dizzy spells.
H2 antihistamines, such as cimetidine, famotidine,
Phantom sweating is another form of autonomic neuropathy. It can be observed in patients with nerve damage (following accidents), diabetes mellitus and as a result of sympathectomy. Phantom sweating is a sensation that one is sweating, while the skin remains dry. Sufferers can not distinguish whether it is real sweating or just a sensation. The phenomena is experienced in the anhidriotic, denervated area of the body, presenting an abnormal sympathetic nervous system function.
My diastolic is usually in the mid 70s or 80s which is fine. The dr gets upset when it goes into the high 80's and 90s. I have had it as low as 47 on occasion and frequently in the 60s. I haven't heard that it is bad to have a low diastolic - why is that? I do know that on diagnosis of hypertension my diastolic was near to 100 and the dr was very worried at that. So although I can't answer your question I am most interested to know what others say.
A regularly occurring dry cough after running is often brought on by exercise-induced asthma, also known as exercise-induced bronchospasms. A respiratory infection could also result in a dry cough, so consult with your doctor for proper treatment. Your doctor can diagnose your symptoms by observing your breathing before and after physical exertion.
The symptoms of exercise-induced asthma, or EIA, typically occur 10 to 15 minutes after you stop running; however, you can experience symptoms during physical exertion as well. A dry cough accompanied by chest tightness and difficulties catching your breath are common symptoms of this form of asthma. You may also experience wheezing and fatigue. The symptoms typically disappear gradually as you rest.
"His acid reflux was diagnosed because of low oxygen saturation levels at a cardiologist appt at the time."
Subarachnoid hemorrhage can be caused by:
Bleeding from a tangle of blood vessels called an arteriovenous malformation (AVM)
Bleeding disorder
Bleeding from a cerebral aneurysm
Head injury
Unknown cause (idiopathic)
Use of blood thinners
Your doctor will likely examine your ears and listen to the blood flow through the arteries in your neck. He or she will listen for an unusual sound that blood makes when it rushes past an obstruction. If your doctor hears this sound, you’ll likely need a test to look for a narrowing or malformation in your carotid artery — and possibly surgery to correct the problem
Pain in your arms, neck, jaw, shoulder, or back accompanying chest discomfort (These symptoms often occur during physical exertion, emotional stress, or eating.)
Tingling, aching, or numbness in the elbows, arms, or wrists (especially your left arm)
STEMI diagnosis was based on electrocardiogram (EKG) criteria including ST-segment elevation of ≥1 mm (0.1 mV) in 2 or more adjacent limb leads or >2 mm in the precordial leads and positive cardiac biomarkers (troponin/CK-MB). Patients with insufficient or unclear data regarding symptom onset or <1 year of follow-up were excluded.
Have you ever felt like your heart has skipped a beat? This may have been an ectopic heartbeat.
Another characteristic symptom of ectopic heartbeats is an occasional feeling of strong forceful beats
On Wednesday, we challenged Well readers to figure out the diagnosis for a middle-aged woman with a pulsating whooshing sound in her head and a sharp stabbing pain on the left side of her neck and head. Nearly 400 readers wrote in with some very thoughtful assessments of this patient’s problem.
The correct diagnosis is…
Hemicrania continua
The only right answer we got came in around 11:15 a.m. from Sashank Prasad, a neuro-ophthalmologist from Brigham and Women’s Hospital in Boston. He says he sees a lot of headache patients because eye involvement is a common feature in many chronic headaches. It was a comment I had made to another reader, noting that the patient didn’t require surgery to get better, that helped him focus on hemicrania continua as the cause of this patient’s pain. One of the characteristics of this syndrome is that it is usually very sensitive to indomethacin, a type of medicine in the same family as ibuprofen and naproxen.
The Diagnosis:
Hemicrania continua is a type of daily headache first described in the early 1980s. It is characterized by the symptoms noted by this patient: persistent pain on one side of the head interspersed with episodes of much more severe pain that is often described as sharp or stabbing. The episodes are usually accompanied by other facial symptoms, including watery eyes, runny nose, eyelid swelling or constriction of the pupil.
Most patients with this type of headache improve when treated with indomethacin. A hemicrania continua headache will sometimes respond to other anti-inflammatory drugs — but response to indomethacin, in particular, is a defining characteristic of the syndrome.
It’s seen more commonly in women than in men and most commonly comes on in a patient’s 20s, though these headaches can start at any age.
How the Diagnosis Was Made:
When the patient came back to the office a few weeks later, I examined her and told her that I thought that she had something known as carotidynia, a pain syndrome caused by inflammation of the tissues of the carotid artery. The cause is unknown, but the condition most frequently occurs in patients with a history of migraine headaches. It is sometimes associated with an injury to the carotid, like a dissection or tumor, but several scans had not detected a problem like that. I had also read that carotidynia and pulsatile tinnitus were more common in patients with abnormal carotid arteries, and this patient, as I described in my previous post, had unusual twisting and meandering carotid arteries.
Carotidynia can usually be treated with medications used to prevent migraine headaches. The patient had already tried beta blockers, the most commonly used migraine preventing drug, but hadn’t tolerated it, so I suggested she try Topamax, a medication developed to prevent seizures, which has also been used successfully to prevent migraines. If these types of medications didn’t work, I told her, we could consider trying a nerve-blocking injection to the region. The patient left my office optimistic that finally she might have found a diagnosis and a treatment. She made an appointment to come back in a month.
A Lucky Break:
Meanwhile, back at the ranch, I was busy studying. Every 10 years internists have to take a test to maintain our certification with the American Board of Internal Medicine. It’s one way the board has to make sure we all stay up to date on the newest medical practices. I had been studying for the past 18 months to take this daylong test in November 2011.
As I was reading, I came across a reference to an unusual disease with a Victorian-sounding name. I didn’t remember it and went to Google to read more about it: hemicrania continua. The first site I clicked on was written by a patient who suffered from this disorder.
And suffer she had. Reading her symptoms was like talking with my patient. The headache was unilateral, constant, stabbing. As I moved on to the medical literature, I saw that my patient’s symptoms fulfilled all the diagnostic criteria for the diagnosis except for one. Patients with this disorder usually have eye symptoms like watery eyes, swollen eyelids or a unilateral constriction of the pupil.
Talking With the Patient:
Excited by my discovery, I couldn’t wait until our next appointment, so I called the patient. How was the Topamax working? I asked. Not so well, she told me. She had stopped taking it after a couple of weeks. It didn’t help the pain, and when she took it she felt “dumb as a rock.”
I told her that I had some new ideas about what might be causing her pain, but first I had a couple of questions. Did she have any eye watering or eyelid swelling when the pain in her head was most intense? Yes, she told me. Sometimes she felt as if she had a cold, just in her left eye. And did she ever notice anything different about the pupil in that eye? Yes, she said. When the pain was most severe she noticed that her pupils were often not the same size. No one had asked her about these symptoms, and they were so mild she hadn’t thought to mention them.
Now I was really excited. I explained my incidental finding and started her on a two-week course of indomethacin. If this was hemicrania continua, she would get better with this medication. I hung up the phone and mentally crossed my fingers.
How the Patient Fared:
A few weeks later we spoke again. How was she feeling? How was her headache? She laughed at the question. She felt great, she told me. Her voice was excited. Her joy was audible.
The headache was gone. Completely gone. She had taken the medicine for almost a week with no effect and had almost given up, when suddenly the headache just disappeared. Just like that. It was amazing, she told me.
Strangely, for reasons I can’t explain, the whooshing sound in her head also disappeared. It had been diminishing over the past several weeks, even before she started the new medication, and now she heard it only occasionally when she held her head in certain positions.
She stopped the indomethacin after the two-week course. Her headaches hadn’t returned. But if they did, she told me, she knew what to do. She told me that she felt normal for the first time in years. Her blood pressure was well controlled on a single medication, but she’s hopeful that once she gets back into shape, she may not need it. In fact, she was getting ready to go for a hike. After not being able to exercise for years, she was working hard to get back into shape and back to her previous level of activity.
There’s a great line in baseball that I used to hear frequently quoted in my first career, when I was a television journalist. It was from Lefty Gomez, a New York Yankee. He said he’d rather be lucky than good. I guess that’s true in medicine. It was lucky I was studying. It was lucky I ran across this mention of this half-remembered disease. It’s humbling to know how easily I could have missed this diagnosis. Does it have to be a choice? Lucky or good? Frankly, I’d much rather be both.
Neurologic symptoms included contralateral limb weakness (55%), facial pain (35%), and Horner's syndrome (21%). Eight patients (28%) presented with an acute hemispheric stroke
Long-term follow-up was available for 20 patients: 14 had complete symptom resolution (70%) and five (25%) had partial clinical symptom resolution. Two patients had initial resolution of symptoms, with subsequent recurrence that was successfully managed conservatively. Follow-up imaging revealed luminal patency in 79% of patients with minimal residual stenosis. Two patients developed a small asymptomatic internal carotid aneurysm that did not require treatment. Mean follow-up was 1133.2 days.
Our finding of 80% luminal recovery at a mean time of 11.2 months is consistent.
Carotid dissection may present as a stroke with weakness on one-side of the body, visual disturbance, facial droop, and/or difficulty with speech. If stroke is suspected, the emergency room is the most appropriate setting for evaluation.
Some patients experience a "whooshing" noise in one ear known as pulsatile tinnitus.
Common carotid artery dissection symptoms include:
Sudden head, face or neck pain with associated neurologic symptoms, such as an small pupil on one side and drooping eyelid (Horner's syndrome)
Vision loss in one eye (amaurosis fugax)
It is not uncommon to be asked to see young patients with ischaemic stroke several weeks after the event. Even when arterial dissection is suspected or proved, if the patient has had no further episodes for a month or more it is tempting to prescribe antiplatelet agents rather than submitting the patient for formal anticoagulation. This case shows that disabling stroke can occur as long as five months after the initial dissection; thus anticoagulation should probably be considered even when there is considerable delay in referral. Although empirical, a minimum period of six months on warfarin would seem appropriate. If repeat duplex ultrasound remains abnormal at that time, extension to 12 months may be necessary.
The R wave is normally the easiest waveform to identify on the ECG and represents early ventricular depolarisation.
The R wave may be enlarged with ventricular hypertrophy, a thin chest wall or with an athletic physique. It may be reduced by a variety of mechanisms including obesity.
After the left ventricle contracts, the aortic valve closes and the mitral valve opens, to allow blood to flow from the left atrium into the left ventricle.
As the left atrium contracts, more blood flows into the left ventricle.
When the left ventricle contracts again, the mitral valve closes and the aortic valve opens, so blood flows into the aorta.
Circumflex artery - supplies blood to the left atrium, side and back of the left ventricle.
Left Anterior Descending artery (LAD) - supplies the front and bottom of the left ventricle and the front of the septum.
Our information shows that 2 causes of Decreased oxygen saturation are related to diabetes, or a family history of diabetes (from a list of 37 total causes)
Myocardial infarction
Tuberculosis
Fibromuscular dysplasia, a segmental, nonatheromatous vascular disease that often leads to stenosis, can cause pulsatile tinnitus, particularly in younger persons. Stenoocclusive vascular diseases found mainly in younger patient groups also include vascular dissection: The vascular lumen is narrowed by a hematoma on the vessel wall. Patients usually complain of acute-onset pain in the back of the neck. Damage to the cervical sympathetic trunk running alongside the vessels leads to ipsilateral Horner syndrome. There is a risk of cerebral infarction resulting from cerebral thromboembolism or hemodynamic instability of cerebral circulation. Angiography reveals tears of the intima, with membranes and intimal cusps, or segmental narrowings of the lumen over longer distances, caused by the intramural hematoma. Magnetic resonance imaging (MRI) often reveals this intramural bleeding directly (Figure 1). In late stages, pseudoaneurysms may form at the location of the intimal tear (7).
The carotid and vertebral arteries are most commonly affected. Middle and distal regions of the internal carotid arteries are frequently involved.[1] Patients with FMD in the carotid arteries typically present around 50 years of age.[3] Symptoms of craniocervical involvement include headaches (mostly migraine), pulsatile tinnitus, dizziness, and neck pain, although patients are often asymptomatic. On physical examination, one may detect neurological symptoms secondary to a stroke or transient ischemic attack (TIA), a bruit over an affected artery, and diminished distal pulses. Complications of cerebrovascular FMD include TIA, ischemic stroke, Horner syndrome, or subarachnoid hemorrhage.[1][2][3]
Sick sinus syndrome comprises a variety of conditions involving sinus node dysfunction and commonly affects elderly persons. While the syndrome can have many causes, it usually is idiopathic. Patients may experience syncope, pre-syncope, palpitations, or dizziness; however, they often are asymptomatic or have subtle or nonspecific symptoms. Sick sinus syndrome has multiple manifestations on electrocardiogram, including sinus bradycardia, sinus arrest, sinoatrial block, and alternating patterns of bradycardia and tachycardia (bradycardia-tachycardia syndrome). Diagnosis of sick sinus syndrome can be difficult because of its nonspecific symptoms and elusive findings on electrocardiogram or Holter monitor. The mainstay of treatment is atrial or dual-chamber pacemaker placement, which generally provides effective relief of symptoms and lowers the incidence of atrial fibrillation, thromboembolic events, heart failure, and mortality, compared with ventricular pacemakers.
Symptoms, which may have been present for months or years, can include syncope, palpitations, and dizziness, as well as symptoms caused by the worsening of conditions such as congestive heart failure, angina pectoris, and cerebral vascular accident.8 Peripheral thromboembolism and stroke, which can occur in the presence of bradycardia-tachycardia syndrome (alternating bradyarrhythmias and tachyarrhythmias), may be related to dysrhythmia-induced emboli.3 A slow heart rate in the presence of fever, left ventricular failure, or pulmonary edema may be suggestive of sick sinus syndrome.2,9 Associated tachycardia may cause flushing of the face, pounding of the heart, and retrosternal pressure.10 Other symptoms include irritability, nocturnal wakefulness, memory loss, errors in judgment, lethargy, lightheadedness, and fatigue2,11 (Table 2).3 More subtle symptoms include mild digestive disturbances, periodic oliguria or edema, and mild intermittent dyspnea.2
Pulmonary edema is typically caused by heart problems brought on by pneumonia, exposure to certain toxins and medications, trauma to the chest wall and exercising or living at high elevations
Following its discovery in the late 19th century, theobromine was put to use by 1916, when it was recommended by the publication Principles of Medical Treatment as a treatment for edema (excessive liquid in parts of the body), syphilitic angina attacks, and degenerative angina.[23]
About 50% of runners had some level of pulmonary edema at about 20-minutes post-race. 20% of those runners had moderate to severe pulmonary edema. Pulmonary edema was still present 1 hour after the marathon was completed.
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Compared to controls, endurance athletes displayed the greatest difference in diameter in the brachial artery (δ = 1.84, 95% CI: 0.59, 3.09, p < 0.01), whereas for mixed athletes, the greatest difference in diameter occurred in the femoral artery (δ = 3.65, 95% CI: 2.21, 5.10, p < 0.01), despite there being no differences in height or body mass between these groups. Resistance athletes had a significantly greater body mass (p = 0.047) and aortic diameter (δ = 1.81, 95% CI: 1.58, 2.05, p < 0.01) than controls, however differences in other vessels could not be determined through meta-analysis due to insufficient data.
The consumption of cocoa and dark chocolate is associated with a lower risk of CVD, and improvements in endothelial function may mediate this relationship. Less is known about the effects of cocoa/chocolate on the augmentation index (AI), a measure of vascular stiffness and vascular tone in the peripheral arterioles. We enrolled thirty middle-aged, overweight adults in a randomised, placebo-controlled, 4-week, cross-over study. During the active treatment (cocoa) period, the participants consumed 37 g/d of dark chocolate and a sugar-free cocoa beverage (total cocoa = 22 g/d, total flavanols (TF) = 814 mg/d). Colour-matched controls included a low-flavanol chocolate bar and a cocoa-free beverage with no added sugar (TF = 3 mg/d). Treatments were matched for total fat, saturated fat, carbohydrates and protein. The cocoa treatment significantly increased the basal diameter and peak diameter of the brachial artery by 6% (+2 mm) and basal blood flow volume by 22%. Substantial decreases in the AI, a measure of arterial stiffness, were observed in only women. Flow-mediated dilation and the reactive hyperaemia index remained unchanged. The consumption of cocoa had no effect on fasting blood measures, while the control treatment increased fasting insulin concentration and insulin resistance (P= 0·01). Fasting blood pressure (BP) remained unchanged, although the acute consumption of cocoa increased resting BP by 4 mmHg. In summary, the high-flavanol cocoa and dark chocolate treatment was associated with enhanced vasodilation in both conduit and resistance arteries and was accompanied by significant reductions in arterial stiffness in women.
The cardiovascular benefits of light to moderate red wine consumption often have been attributed to its polyphenol constituents. However, the acute dose-related hemodynamic, vasodilator, and sympathetic neural effects of ethanol and red wine have not been characterized and compared in the same individual. We sought to test the hypotheses that responses to one and two alcoholic drinks differ and that red wine with high polyphenol content elicits a greater effect than ethanol alone. Thirteen volunteers (24-47 yr; 7 men, 6 women) drank wine, ethanol, and water in a randomized, single-blind trial on three occasions 2 wk apart. One drink of wine and ethanol increased blood alcohol to 38 +/- 2 and 39 +/- 2 mg/dl, respectively, and two drinks to 72 +/- 4 and 83 +/- 3 mg/dl, respectively. Wine quadrupled plasma resveratrol (P < 0.001) and increased catechin (P < 0.03). No intervention affected blood pressure. One drink had no heart rate effect, but two drinks of wine increased heart rate by 5.7 +/- 1.6 beats/min; P < 0.001). Cardiac output fell 0.8 +/- 0.3 l/min after one drink of ethanol and wine (both P < 0.02) but increased after two drinks of ethanol (+0.8 +/- 0.3 l/min) and wine (+1.2 +/- 0.3 l/min) (P < 0.01). One alcoholic drink did not alter muscle sympathetic nerve activity (MSNA), while two drinks increased MSNA by 9-10 bursts/min (P < 0.001). Brachial artery diameter increased after both one and two alcoholic drinks (P < 0.001). No beverage augmented, and the second wine dose attenuated (P = 0.02), flow-mediated vasodilation. One drink of ethanol dilates the brachial artery without activating sympathetic outflow, whereas two drinks increase MSNA, heart rate, and cardiac output. These acute effects, which exhibit a narrow dose response, are not modified by red wine polyphenols.
Pleiotropic effects of garlic [Original article in German]
Siegel G, Walter A, Engel S, Walper A, Michel F.
Institut fur Physiologie, Universitatsklinikums Benjamin Franklin, Freien Universitat Berlin, Deutschland. siegel@mail.grumed.fu-berlin.de
Garlic as a herbal remedy reduces a multitude of risk factors which play a decisive role in the genesis and progression of arteriosclerosis: decrease in total and LDL-cholesterol, increase in HDL-cholesterol, reduction of serum triglyceride and fibrinogen concentration, lowering of arterial blood pressure and promotion of organ perfusion, and, finally, enhancement in fibrinolysis, inhibition of platelet aggregation, and diminution of plasma viscosity. In a prospective, 4-year clinical trial with primary endpoint ‘arteriosclerotic plaque volume’ it was proven not only a 9 to 18% reduction and 3% regression in plaque volume of the total collective under the influence of standardized garlic powder dragees (900 mg/die LI 111), but also of some facets of the phytopharmacologic pleiotropy of this herb: decrease in LDL level by 4%, increase in HDL concentration by 8%, and lowering in blood pressure by 7%. The reduction of arterial blood pressure is due to an additional opening of K(Ca) ion channels in the membrane of vascular smooth muscle cells that effects its hyperpolarization. This membrane hyperpolarization closes about 20% of the L-type Ca2+ channels, consequence of which is vasodilatation. In human coronary arteries, the increase in vascular diameter by 4% is closely associated with an improvement of coronary perfusion by 18%. These pleiotropic effects of garlic result in a reduction of relative cardiovascular risk for infarction and stroke by more than 50%.
We measured serum lipoproteins and glucose and brachial artery flow-mediated vasodilation (FMD), an index of endothelial function, before and 3 h after each meal.RESULTSAll five meals significantly raised serum triglycerides, but did not change other lipoproteins or glucose 3 h postprandially. The olive oil meal reduced FMD 31% (14.3 ± 4.2% to 9.9 ± 4.5%, p = 0.008). An inverse correlation was observed between postprandial changes in serum triglycerides and FMD (r = −0.47, p < 0.05). The remaining four meals did not significantly reduce FMD
1999 study measuring FMD after the ingestion of high-fat meals reported a “3-hour decline in FMD after subjects ingested a traditional meal of a hamburger and fries or cheesecake. Olive oil was found to have the same impairment to endothelial function as the rest of these high-fat meals.”
And a 2007 study showed a similar detrimental effect on endothelial function after the intake of olive, soybean and palm oils. - Read more at: http://scl.io/FqAWY3yy#gs.9mSQolU
a cohort study designed to measure the effects of a Mediterranean diet as the primary prevention of cardiovascular disease, extra virgin olive oil (EVOO) was shown to be better than regular olive oil, but neither significantly reduced heart attack rates.
Other studies report similar findings, showing that EVOO damages endothelial function—just like its ‘regular’ olive oil counterpart.
In the PREDIMED study, 7447 people at high risk for cardiovascular disease were randomly placed into 3 groups. One group was told to eat a Mediterranean diet using only EVOO (up to 1 liter per week!). The second group ate a Mediterranean diet and added half-pound of nuts per week. The third group was told to reduce fat intake (but it didn’t).
After five years, the conclusions were stunning; there were nearly no differences between groups. No differences in weight, waist circumference, systolic and diastolic blood pressure, fasting glucose, or lipid profile.
And no difference in the number of heart attacks or deaths from cardiovascular disease; those in the EVOO group suffered just as many heart attacks and cardiovascular disease as those in the control group (there was a significant reduction in the number of strokes, but that reduction was greater in the group that ate nuts). - Read more at: http://scl.io/FqAWY3yy#gs.9mSQolU
Mean (+/- SD) baseline characteristics were age 62 +/- 7 years, plasma total cholesterol concentration 187 +/- 31 mg/dl (4.83 +/- 0.80 mmol/liter) and triglyceride levels 132 +/- 70 mg/dl (1.51 +/- 0.80 mmol/liter). Fish oil lowered triglyceride levels by 30% (p = 0.007) but had no significant effects on other plasma lipoprotein levels. At the end of the trial, eicosapentaenoic acid in adipose tissue samples was 0.91% in the fish oil group compared with 0.20% in the control group (p < 0.0001). At baseline, the minimal lumen diameter of coronary artery lesions (n = 305) was 1.64 +/- 0.76 mm, and percent narrowing was 48 +/- 14%. Mean minimal diameter of atherosclerotic coronary arteries decreased by 0.104 and 0.138 mm in the fish oil and control groups, respectively (p = 0.6 between groups), and percent stenosis increased by 2.4% and 2.6%, respectively (p = 0.8). Confidence intervals exclude improvement by fish oil treatment of > 0.17 mm, or > 2.6%.
Fish oil treatment for 2 years does not promote major favorable changes in the diameter of atherosclerotic coronary arteries.
When considering cardiovascular health, it seems premature to recommend general usage until compelling evidence for the beneficial action of fish oil supplements is at hand. Although doses of 3 to 8 g of n-3 PUFA per day in those with CHD were not associated with significant adverse effects in recent clinical trials,8 34 evidence for beneficial effects in CHD patients is either lacking or needs additional study. Currently, fish oil capsules can only be recommended for the infrequent patients with severe, treatment-resistant hypertriglyceridemia who are at increased risk for pancreatitis. Potential side effects should be kept in mind (Table⇓1 40 ). On the other hand, inclusion of marine sources of the n-3 PUFA in the diet seems reasonable because they are good sources of protein without the accompanying high saturated fat seen in fatty meat products. Moreover, as Harris has noted, the potential for benefit remains high, since dietary fish oils affect “a myriad of potentially atherogenic processes.”41 This requires the continued support of cardiovascular research on the n-3 PUFA.
there was no significant relationship between
fish consumption and FMD, after accounting
for age, gender, race
– ditto for plasma EPAHA and FMD
Importantly, caffeinated coffee intake significantly enhanced post-occlusive reactive hyperemia of finger blood flow, an index of microvascular endothelial function, compared with decaffeinated coffee intake.
An increase in nitrate intake can augment circulating nitrite and nitric oxide. This may lead to lower blood pressure and improved vascular function. Green leafy vegetables, such as spinach, are rich sources of nitrate. We aimed to assess the acute effects of a nitrate-rich meal containing spinach on arterial stiffness and blood pressure in healthy men and women. Twenty-six participants aged 38-69years were recruited to a randomized controlled cross-over trial. The acute effects of two energy-matched (2000kJ) meals, administered in random order, were compared. The meals were either high nitrate (220mg of nitrate derived from spinach [spinach]) or low nitrate [control]. Outcome measurements were performed pre-meal and at specific time points up to 210min post meal. Spinach resulted in an eightfold increase in salivary nitrite and a sevenfold increase in salivary nitrate concentrations from pre-meal (P<0.001) to 120min post meal. Spinach compared with control resulted in higher large artery elasticity index (P<0.001), and lower pulse pressure (P<0.001) and systolic blood pressure (P<0.001). Post meal carotid-femoral pulse wave velocity (P=0.07), augmentation index (P=0.63), small artery elasticity index (P=0.98) and diastolic blood pressure (P=0.13) were not significantly altered by spinach relative to control. Therefore, consumption of a nitrate-rich meal can lower systolic blood pressure and pulse pressure and increase large artery compliance acutely in healthy men and women. If sustained, these effects could contribute to better cardiovascular health.
In conclusion, the present study shows that there is no vascular effect demonstrable by the measurement of FMD after intervention with tomato purée for 7 d in healthy postmenopausal women
The pooled analysis of seven prospective studies, with 116,127 participants and 1,989 cases, demonstrated that lycopene decreased stroke risk by 19.3% (RR = 0.807, 95% CI = 0.680–0.957) after adjusting for confounding factors.
. Upon simultaneous analyses of the carotenoids, however, using conditional logistic regression models that controlled for age, body mass index, socioeconomic status, smoking, hypertension, and maternal and paternal history of disease, lycopene remained independently protective, with an odds ratio of 0.52 for the contrast of the 10th and 90th percentiles (95% confidence interval 0.33-0.82, p = 0.005)
The HS reference diet used full-fat milk (3.8 g/100 mL) and cheese (35 g/100 g), whereas these were replaced with skimmed milk (0.1 g fat/100 g) and half-fat cheese (18 g/100 g) in HM and HC diets.
FMD with the HS reference diet was 6.7 ± 2.2%, and changes (95% CIs) after 6 mo of intervention were +0.3 (−0.4, 1.1), −0.2 (−0.8, 0.5), and −0.1 (−0.6, 0.7) with HS, high-MUFA (HM), and high-carbohydrate (HC) diets
With the HS reference diet, the geometric mean (±SD) plasma 8-isoprostane F2α-III concentration was 176 ± 85 pmol/L, and mean percentage of changes (95% CIs) were 1 (−12, 14) with the HS diet, 6 (−5, 16) with the HM diet, and 4 (−7, 16) with the HC diet.
Ultimately, Fleming decided to publish his findings and move on to another category of "anti-biotic," sulpha drugs – dyes that on a good day poison bacteria, but on most days poison the patient.
The AAD provided 8.7% energy from PUFA (7.7% LA, 0.8% ALA). On the LA diet, saturated fat was reduced, and PUFA from walnuts and walnut oil provided 16.4% of energy (12.6% LA, 3.6% ALA). On the ALA diet, walnuts, walnut oil, and flax oil provided 17% energy from PUFA (10.5% LA, 6.5% ALA).
The ALA and LA diets significantly reduced diastolic blood pressure (−2 to −3 mm Hg) and total peripheral resistance (−4%), and this effect was evident at rest and during stress (main effect of diet, p < 0.02). FMD increased (+34%) on the diet containing additional ALA. AVP also increased by 20%, and endothelin-1 was unchanged.
During the ALA diet only, FMD increased by 34% relative to the control diet (p = 0.05; Table 4).
Diets included an average American diet (AAD) that served as the control (based on typical U.S. intake of macronutrients [19]) and 2 experimental diets high in total PUFA and low in saturated fat.
Compared with the olive oil–rich meal during the control diet, the walnut meal during the walnut diet significantly (P=0.043) improved EDV from 3.6±3.3% to 5.9±3.3%, a relative increase of 64% (the Figure and Table 2).
Resting and hyperemic brachial artery diameter did not change either with tea or with caffeine. FMD increased significantly with tea (by 3.69%, peak at 30 min, P<0.02), whereas it did not change significantly with caffeine (increase by 1.72%, peak at 30 min, P=NS). Neither tea nor caffeine had any effect on high-sensitivity C-reactive protein, Il-6, Il-1b, total plasma antioxidative capacity, or total plasma oxidative status/stress.
When the results of patients randomized to tea first and water first were combined, flow-mediated dilation was 6.0±3.4% at baseline, 5.7±3.9% after short-term water, 6.1±4.3% after long-term water, 9.4±3.9% after short-term tea, 9.5±3.6% after long-term tea, and 10.8±4.4% after short–on–long-term tea.
Flow-mediated dilation with short–on–long-term tea consumption was comparable to that of healthy volunteers in our laboratory (11.2±5.7%).24 These findings suggest that tea consumption reverses endothelial vasomotor dysfunction in patients with CAD and are comparable to our recent findings with the antioxidant ascorbic acid.
Tea consumption had no effect on baseline diameter, extent of reactive hyperemia, or nitroglycerin-induced vasodilation, suggesting that tea acted to improve endothelial vasomotor function rather than acting to alter resting vascular tone, increase the stimulus for dilation, or improve vascular smooth muscle function.
http://www.sciencedirect.com/science/article/pii/S0019483215008299
FMD as surrogate marker of endothelial function was comparable at the end of the study in both groups (Table 6).
The first meal contained safflower oil (fatty acid composition: 75% polyunsaturated, 13.6% monounsaturated, and 8.8% saturated fat). The second meal contained coconut oil (fatty acid composition: 89.6% saturated fat, 5.8% monounsaturated, and 1.9% polyunsaturated fat)
Consumption of a saturated fat reduces the anti-inflammatory potential of HDL and impairs arterial endothelial function. In contrast, the anti-inflammatory activity of HDL improves after consumption of polyunsaturated fat. These findings highlight novel mechanisms by which different dietary fatty acids may influence key atherogenic processes.
Post-hyperemic forearm blood flow increased 3 h after consumption of the polyunsaturated fat by 45 ± 14% and by 21 ± 11% after the saturated fat meal (Table 3). Flow-mediated dilation (FMD) decreased at 3 h following consumption of the saturated meal (p < 0.05 compared with pre-meal) but not 3 h after the polyunsaturated meal (p = NS compared with the fasting state). The FMD at 6 h after both meals did not significantly differ compared with the fasted state (Table 4), There was no significant change in the vessel size, estimated flow within the brachial artery, and glyceryl trinitrate response following both meals.
One study conducted by Dr. Thomas Wang revealed that individuals with low vitamin D levels had a 60% increase in incidence of heart attacks and strokes. The theory behind this could be postulated to Vitamin D reducing arterial calcification by diverting calcium to bones and teeth instead of soft tissues such as the arteries. Arterial calcifications reduce the diameter of the arteries, for example in the coronary arteries, causing a diminished flow of blood to areas of the heart muscle supplied by the coronary arteries.
Analysis of brachial artery diameters showed that the mean of baseline diameters did not statistically change after the intervention (P > 0.999).
FMD analysis showed that after vitamin D injection, FMD was significantly increased (P < 0.001) (table 2). Split analysis of patients with vitamin D deficiency and those with insufficiency provided the same results; FMD was improved in both groups (P < 0.001).