Prodigal Son said:In terms of 'buzz' and quantities of coffee, I've found that it depends on the brand/mix of coffee (at the moment I'm only on organic instant granules). Next, I'll invest in a cafetiere and grind some beans and see what happens with that. :) Learning is fun! :D
Prodigal Son said:It is recommended that you drink coffee in the morning to allow the 'stimulant' effects to get through your system before you go to sleep. I usually drink it after my breakfast drink of broth, which is after my bacon or pork sausageandi said:...
I don't sleep as well either as when I don't have coffee, maybe I'm having some too late (6-7pm).
Role of DAT-SPECT in the diagnostic work up of parkinsonism.
_http://www.ncbi.nlm.nih.gov/pubmed/17486648
The diagnosis of idiopathic Parkinson's disease (PD) can be achieved with high degrees of accuracy in cases with full expression of classical clinical features. However, diagnostic uncertainty remains in early disease with subtle or ambiguous signs. Functional imaging has been suggested to increase the diagnostic yield in parkinsonian syndromes with uncertain clinical classification. Loss of striatal dopamine nerve terminal function, a hallmark of neurodegenerative parkinsonism, is strongly related to decreases of dopamine transporter (DAT) density, which can be measured by single photon emission computed tomography (SPECT). The use of DAT-SPECT facilitates the differential diagnosis in patients with isolated tremor symptoms not fulfilling PD or essential tremor criteria, drug-induced, psychogenic and vascular parkinsonism as well as dementia when associated with parkinsonism. This review addresses the value of DAT-SPECT in early differential diagnosis, and its potential as a screening tool for subjects at risk of developing PD as well as issues around the assessment of disease progression.
"Multiple roles for nicotine in Parkinson’s disease"
_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815339/
The basal ganglia are key in the pathogenesis of Parkinson’s disease, a movement disorder characterized by a predominant loss of nigrostriatal dopaminergic neurons [1-3]. A major component of the basal ganglia is the striatum which receives projections from dopaminergic cell bodies in the substantia nigra. In addition to dopamine, the striatum contains a wide diversity of neuroactive substances including serotonin, glutamate, GABA, noradrenaline, cannabinoids, opioids, adenosine, and numerous neuropeptides, any of which may contribute to the regulation of dopaminergic activity [4-18]. Furthermore, extensive evidence shows that acetylcholine influences striatal dopamine release predominantly through an action at nAChRs [19-21], and also muscarinic receptors to a lesser extent [22-24]. These interactions of acetylcholine at the cellular level most likely have important behavioral consequences.
SPECT Molecular Imaging in Parkinson's Disease
_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321451/
Motor symptoms such as tremor at rest, akinesia, rigidity, and postural instability are the cardinal signs in PD [6]. The type and severity of symptoms experienced by a person with PD vary with each individual and the stage of the disease. PD is the most common cause of parkinsonism. There are also many nonmotor features of PD including behavioral and psychiatric problems such as dementia [7], fatigue [8], anxiety [9] and depression [10], autonomic dysfunction [11], addiction and compulsion [12], psychosis [13], olfactory dysfunction [14], and cognitive impairment [10]. These clinical features also occur in other neurodegenerative diseases and by dopamine receptor antagonist drugs, which means that with this main clinical application it is hard to diagnose patients with mild, incomplete, or uncertain parkinsonism [15]. The United Kingdom Parkinson's Disease Society Brain Bank clinical diagnostic criteria can improve diagnostic accuracy [16]; still, the diagnosis and management of PD can be a challenge.
The diagnosis of PD is based on clinical criteria, but misdiagnosis is as high as 25% of cases as confirmed by anatomic-pathologic studies. Because the diagnosis of PD is entirely clinical, the diagnosis and treatment may be delayed for years until functional disability occurs. SPECT is an aid that can help diagnosing the disease earlier.
Neuroimaging in Parkinson’s Disease
_http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3075732/
Parkinson’s disease (PD) is a common disorder in which the primary features can be related to dopamine deficiency. Changes on structural imaging are limited, but a wealth of abnormalities can be detected using positron emission tomography, single photon emission computed tomography, or functional magnetic resonance imaging to detect changes in neurochemical pathology or functional connectivity. The changes detected on these studies may reflect the disease process itself and/or compensatory responses to the disease, or they may arise in association with disease- and/or treatment-related complications. This review will focus mainly on neurochemical and metabolic studies and reviews various approaches to the assessment of dopaminergic function as well as the function of other neurotransmitters that may be affected in PD. A number of clinical applications are highlighted, including diagnostic utility, identification of preclinical disease, changes associated with motor and nonmotor complications of PD, and the effects of various therapeutic interventions.
Parkinson’s disease (PD) is the second most common neurodegenerative disorder, estimated to affect 200–300 per 100,000 population. While other areas of both the central and peripheral nervous system may be affected, [1] the most important pathological finding in PD is the loss of dopaminergic neurons in the substantia nigra that project to the striatum, most often associated with cytoplasmic Lewy bodies. The symptoms of PD do not appear until approximately 50% of the nigral dopamine (DA) neurons have been lost, but the impact on routine structural imaging findings is minimal at this stage. Consequently, structural imaging has in general been unrewarding, although some newer MRI techniques, such as diffuse tensor imaging or shape analysis, are somewhat more promising. Despite the relatively limited structural changes, it is estimated that there is an approximately 80% decline of striatal DA before typical motor symptoms appear, and this has substantial functional effects on the cortical–striatal–pallidal–thalamic–cortical circuitry. PD is therefore an ideal condition for the application of functional imaging techniques, and findings from these will form the thrust of this review. These techniques may not only shed insights into PD and the basis for its complications, but they may also be useful for deriving inferences regarding the role of DA in the normal brain.
Cognitive and behavioral complications
Deficits in executive function are common in PD, even in the absence of dementia. Cognitive dysfunction in PD is associated with a glucose metabolic pattern of reduced activity in the frontal and parietal cortex as well as increased activity in the cerebellar vermis [104] and is independent of the PDRP described above and unresponsive to levodopa. Dementia in PD is associated with marked reductions in glucose metabolism in the occipital cortex, a pattern distinct from that seen in Alzheimer disease [105]. PD is also associated with widespread deficits in cholinergic activity, and these are more pronounced in patients with dementia, exceeding the abnormalities seen in Alzheimer disease [106]. A few studies have used 11C-labeled Pittsburgh Compound B to assess amyloid deposition in PD with dementia. For the most part, these studies suggest that amyloid deposition is increased in subjects with Lewy body dementias, but not in those with PD-dementia [107, 108]. Many investigators consider these to represent variations of the same disorder, and this distinction may accordingly be seen as somewhat surprising. Another recent study suggests that amyloid deposition in both Lewy body dementias and PD-dementia is related to expression of the ApoE4 allele [109].
Depression affects approximately 40–50% of patients with PD [110] and may antecede motor dysfunction [111, 112].
A diagnosis of PD can be made when someone has at least two of the three cardinal signs — rest tremor, rigidity, and bradykinesia (abnormal slowness of movement). Tremor is present in 85% of people with true PD. The gradual onset of symptoms further supports the diagnosis. Masked facies, decreased eye blinking, stooped posture, and decreased arm swing complete the early picture. The onset may also be preceded by vague feelings of weakness and fatigue, incoordination, aching, and discomfort.
Other aspects of PD include depression and anxiety, cognitive impairment, sleep disturbances, sensory abnormalities and pain, loss of smell (anosmia), and disturbances of autonomic function which can produce diverse manifestations, including postural low blood pressure, constipation, urinary urgency and frequency, excessive sweating, and seborrhea. Some of these other aspects may be present long before the onset of movement/motor signs. The physiologic basis of the non-motor signs and symptoms are explained in part by widespread involvement of brainstem, olfactory, thalamic, and cortical structures in the brain.
Sensory symptoms most often manifest as a distressing sensation of inner restlessness presumed to be a form of akathisia (Intense anxiety at the thought of sitting down; inability to sit down). Sleep disorders are common in PD.
Changes in mood, cognition, and behavior are common accompaniments of the later stages of PD. Depression affects approximately half of patients with PD and can occur at any phase of the illness. Anxiety disorders in PD can appear in isolation or as an accompaniment of depression or progressive cognitive impairment. They can also be due to a "dopamine hunger”. Cognitive abnormalities affect many patients with PD. Most are mild to moderate in severity. Difficulties with complex tasks, long-term planning, and memorizing or retrieving new information are common. Although some of these symptoms represent bradyphrenia (the cognitive equivalent of bradykinesia, slowness of movement), it is now clear that the dysfunction also includes working memory, attention, mental flexibility, visuospatial function, word fluency, and executive functions.
In PD dopaminergic and other cells die due to a combination of factors including: (1) genetic vulnerability, (2) oxidative stress [and/or mitochondrial dysfunction] (3) proteosomal dysfunction, and (4) environmental factors.
Louise Hay says that Parkinson's disease is "Fear and an intense desire to control everything and everyone. And perhaps in relation to this, it is interesting that a study suggests that risk takers escape Parkinson's (http://www.sott.net/article/164331-Risk-takers-escape-Parkinsons). Dan Neuharth shared some insights regarding controlling issues in his book about narcissism, "Controlling Parents". He provides some insights in the human aspects of fear:
[Unfortunately, I edited this text. At that time I had the idea to change "Controlling Parents" to "controlling persons" in order to reflect that it was about the person and not about the parents. Perhaps someone has the book and can find the original quote?]
"Fear is a key commonality among controlling persons. Knowing your needs and fears will make you understand why you control, even when you are not aware that you are controlling: fear of being seen as flawed, fear of feeling powerless, fear of feeling invalidated, fear of feeling vulnerable, fear of losing emotional control.
"One of the fascinating aspects of human behavior is that it often compensates in reverse and generally without being aware of it. Someone who feels particularly small may go around acting larger than life. Someone who feels adrift in an emotional rapids may become expressionless. Someone who fears rejection may reject others first. Feeling flawed, controlling persons aimed at being perfect. Feeling small, they act big. Feeling afraid, they frighten others. Feeling bad about themselves, they shame others. Feeling wrong, they insist on being right. Feeling doubt, they confuse. Feeling deprived, they withhold.
"Unconsciously, they adopt myths about themselves: the self-made man, the perfect mom, the good provider, the in-control dad, etc. These myths give them the illusion that they are in total control of their destinies. This may explain why some of them seem disconnected from the present, often unaware of their surroundings and feelings. Living in the moment risks loss of control and lacks guarantees. Controlling persons are often unaware of why they act as they do. If they realized what lay underneath their maladaptive behavior, they'd have to face their dependency on others for their feelings of self-worth, and their desperate hunger for the symbols of success. They'd have to face the fact that they are as controlled as anyone else.
"Controlling persons rarely learned that facing their feelings or admitting their limits can be healing. Because they try to control everything, they tend to think that others are doing the same. Since most controllers want to be sure they are never dominated, they move to control first.
"In short, being a controlling person is a defensive action. A combination of factors - how the controlling person was raised, lack of knowing better, external events, internal needs, and the footprints of trauma/bad experiences, etc - leave controlling persons, unless they get help, playing out a lifelong defensive drama.
"Controlling is a futile effort to secure guarantees that they will be loved and safe rather than powerless, invalidated, or out of control. Yet it is costly because: Persons who fear being judged as flawed can never let others see them as they truly are. Persons who need to feel powerful must always be on guard against threats to their power. Persons who fear invalidation cannot tolerate questions or uncertainty. Persons who fear vulnerability view everything and everyone as potentially threatening. Persons who must avoid feeling out of control are likely to miss out on joy, spontaneity, and love.
_http://www.naturalnews.com/034063_mycotoxins_coffee.html1. Drink coffee that has been made via wet processing. Because mycotoxins often form during the drying process, wet beans are much less likely to contain them than dry beans.
2. Do not drink decaffeinated coffee. Caffeine actually protects coffee beans from the growth of mold and can prevent large amounts of mycotoxins from growing.
3. Choose arabica beans over robusta beans. Though robusta varieties do have higher levels of caffeine, they also contain more mycotoxins.
4. Consider the environment in which your beans are grown. Because mold is less apt to grow at higher elevations, buying beans that have been harvested in the mountains of Central America is a great way to decrease the amount of toxins in your coffee.
5. Stay away from blends. Though blended coffees may taste good, there really is no way of telling where the different bean varieties have come from. Try to stick to single estate products rather than the major brand names.
6. Steam is an agent that can help break down toxins, so if all else fails, order an Americano.
mnmulchi said:Thanks Gandalf for mentioning Oolong tea, I just tried a plain Oolong version and enjoy it as well. It seems like a more complex tasting black tea. There are so many different teas available, it's hard to decide on which ones to try! Never having been a big tea drinker, I'm now finding I prefer the variety of tea flavors, to the taste of coffee.
Laura said:My report on the coffee experiment:
It's hard to tell if it was damaging in any way. What I noted was:
1) a raw feeling in my nasal passages
2) extra phelgm production
3) reduction in urine volume
4) slight weight gain but no visible swelling as on ankles
5) slight improvement in bowel frequency.
6) don't sleep as well even if only have coffee in morning
7) energy slump in afternoon that was previously absent - get very sleepy.
8) slight brain fog once in awhile.
Laura said:My report on the coffee experiment:
It's hard to tell if it was damaging in any way. What I noted was:
1) a raw feeling in my nasal passages
2) extra phelgm production
3) reduction in urine volume
4) slight weight gain but no visible swelling as on ankles
5) slight improvement in bowel frequency.
6) don't sleep as well even if only have coffee in morning
7) energy slump in afternoon that was previously absent - get very sleepy.
8) slight brain fog once in awhile.