Newsletter Subject

Using daffodil flowers to fight Alzheimer’s

From

malehealthcures.com

Email Address

matt@malehealthcures.com

Sent On

Wed, May 19, 2021 07:14 PM

Email Preheader Text

The latest breakthrough for preventing this awful disease ----Important Message From Our Sponsor----

The latest breakthrough for preventing this awful disease ----Important Message From Our Sponsor---- 3 secrets to getting more head (this makes her WANT to go down on you) [Can't see this image? Click on 'load images' or 'always allow images for this sender'] There’s nothing better than when a beautiful woman puts you in her mouth... ...and it’s even better when she’s really into it! I used to think it was virtually impossible to convince a woman to go down on me more often... ...until I discovered how much women truly love giving passionate BJs to the right sort of guy... ...the sort of man who knows how to make her WANT to give you more ​head in the first place... [Discover the 3 little-known secrets to make your wife or girlfriend want to give you all the oral action you can handle (even if she’s said she doesn’t like it)]( ---------- Using daffodil flowers to fight Alzheimer’s Galantamine is an alkaloid isolated from several flower varieties, including the daffodil and the common snowdrop (Galanthus nivalis).  This classic effect of this treatment is to inhibit cholinesterase, the enzyme primarily responsible for degrading acetylcholine. Inhibiting this enzyme prevents the hydrolysis of acetylcholine, and whatever is spared can be used to enhance cognition. Alzheimer's disease is characterized on the molecular level by a few things: Neurofibrillary tangles, β-amyloid deposits, and reduced acetylcholine receptors all define this condition. 'Impairment of cholinergic function in AD contributes to the cognitive deficits that are characteristic of the illness.' ―Raskind Cholinesterase inhibitors are commonly used to treat Alzheimer's disease for these reasons, and are in fact the only class of treatments FDA-approved in doing so. Included in this class are just three treatments which can be legally given out, namely: donepezil, rivastigmine, and galantamine. (The treatment tacrine had formerly been included in this list but was discontinued on account of hepatotoxicity.) Of this set, only galantamine is an all-natural compound and exhibits the safety profile you'd expect from such. All three treatments have a comparable potency and are used in the 10 to 25 milligram range, per day. This is despite the fact that galantamine is the weakest of the three at inhibiting cholinesterase, which implies some other mechanism of action. The doses of galantamine consistently shown to improve cognition are expected to yield only ~10% brain cholinesterase inhibition (Thomsen, 1991). Because galantamine works as well as the other treatments, if not more so, there must be something else to it… This is in fact the case, and galantamine is also a strong modulator of nicotinic acetylcholine receptors (Samochocki, 2003). This other effect of galantamine is actually quite strong. This treatment is technically an allosteric modulator of acetylcholine receptors, functioning in a way not unlike benzodiazepines at GABAA receptors. Allosteric modulators don't actually activate receptors themselves, yet do potentiate the responses of other ligands. This effect can be substantial with certain molecules such as oleamide, for instance, which is capable of increasing the response of .1 μM serotonin at the 5-HT1A receptor at only a 1μM concentration (Boger, 1998). The potency of this natural metabolite -- derived from oleic acid and ammonia -- is so great that it's active through the nanomolar range. You could almost say that oleamide is more serotonergic than serotonin itself. Galantamine is just as potent as any allosteric treatment on nicotinic acetylcholine receptors. Galantamine begins working at around 100nM, giving it comparable potency to oleamide on 5-HT1 and diazepam on GABAA. So in addition to galantamine being the only all-natural treatment approved, and the safest, it is the only one with dual functionality. 'The amplitudes of currents produced by acetylcholine plus galantamine (30 and 0.5 μM, respectively) were similar to those of currents evoked by 1000 μM acetylcholine alone.' ―Samochocki And this also means that galantamine is a prime candidate for being a “nootropic treatment,” despite not generally being considered such. The fact that it inhibits cholinesterase and also modulates acetylcholine receptors makes its inclusion as one all but certain. All of this has been proven. Although there are treatments that perform each of galantamine's two separate functions individually, the cumulative results of the studies below suggest galantamine has unparalleled activity as a single agent. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Although there'd been studies before this point using galantamine on acetylcholine receptors, yet this had been the first one to investigate the interaction in greater detail. They had discovered that galantamine is an allosteric potentiating ligand (APL), a molecule that increases the response of an agonist by binding to a separate site on the receptor. The word allosteric is a Greek compound word that roughly translates into “other site.” This specific function of galantamine had been proven by using an antibody specific to the “APL site,” the addition of which had blocked galantamine's response but had no bearing on those induced by nicotine and acetylcholine. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Galantamine also did not compete with nicotine, acetylcholine, or epibatidine. These findings further suggest that galantamine binds to a separate site than the classic agonists. Yet on account of galantamine being capable of potentiating the response of cholinergic agents in ultra-low concentrations, it must be considered something...if not a true “agonist.” And it is. Galantamine is an official allosteric modulator of nicotinic acetylcholine receptors. This subtyping matters, as muscarinic acetylcholine receptors are what cause most of the side effects observed with excessive acetylcholine levels.  [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Since all common nicotinic treatments are selective to that receptor, it is generally only cholinesterase inhibitors and muscarinic agents that cause nausea and vomiting. Because cholinesterase inhibitors act to increase acetylcholine indiscriminately, the intended nicotinic receptors are activated and the unintended muscarinic ones as well. 'The APL action of galantamine produces a selective nicotinic cholinergic enhancement. In contrast, cholinergic enhancement by ChE inhibition always is both, nicotinic and muscarinic, with the latter enhancement responsible for most of the reported side effects of this therapy.' ―Samochocki Hence atropine -- an antimuscarinic agent -- is often used alongside cholinesterase inhibitors to block acetylcholine's action on muscarinic receptors. Yet galantamine is a relatively weak cholinesterase inhibitor, and because it works at the same dose as donepezil you're nearly forced into assuming the APL effect is primary. These chemists had also used all of the five muscarinic acetylcholine receptor subtypes (M1-M5), and had discovered that galantamine has essentially zero activity on every one of them -- even at massive concentrations (1000μM). They had also shown that all other cholinesterase inhibitors besides physostigmine do not have this secondary APL function on nicotinic acetylcholine receptors (nAChR). [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Neither donepezil, rivastigmine, tacrine, metrifonate, and dichlorvos act as allosteric potentiating ligands (APLs). This demonstrates the uniqueness of galantamine, a selective nicotinic agent that synergizes with itself by increasing the acetylcholine it later potentiates. As an allosteric potentiating ligand, this treatment does not compete with primary nicotinic agents yet greatly amplifies their response. This means that it belongs to a small class that would synergize with, and not compete against, both primary nAChR ligands and other cholinesterase inhibitors. 'In contrast, galantamine (0.5 μM) enhanced by 50 to 60% the response to nicotine of human 42 nAChR-expressing cells.' ―Samochocki This fact is very important as nicotinic acetylcholine receptors (nAChR) are central to cognition, and their deficiency in Alzheimer's is thought to greatly contribute to the condition. Since nicotine is the eponymous ligand of this receptor type, it should be no surprise that smoking has been consistently found protective against Alzheimer's disease (Nitta, 1994). The correlations are strong but aren't perfect, and this could be because many separate forms of dementia are now grouped under the heading of “Alzheimer's disease.” Nicotine probably cannot be expected to work in all cases, specifically those caused by neurofibrillary tangles. Neurofibrillary tangles appear, on all counts, to be a permanent inclusion body induced by aluminum ions (Al3+). Beta-amyloid deposits are another issue altogether, yet there's reason to suppose they are caused by low sulfate groups (SO42−) -- in turn caused by sulfate depleting-treatments such as acetaminophen (Heafield, 1990). 'nAChRs are found in brain areas that are important in the control of cognition and memory, such as the cerebral cortex and hippocampus.' ―Samochocki Yet even in patients having unrelated problems you'd still expect cholinergic agents to improve dementia, at least to some degree. These treatments are what most consistently improve learning in rats, rabbits, monkeys, and humans. For this reason you'd expect a treatment of this type, besides treating dementia, would also be also studied in relation to learning in general. This treatment certainly has, and galantamine can improve learning acquisition in monkeys (Schneider, 2003) and in rabbits (Woodruff-Pak, 2001).  [Can't see this image? Click on 'load images' or 'always allow images for this sender'] This study had tested galantamine under a rigidly-controlled learning paradigm in rabbits at a dose of 3 milligrams per kilogram (b.w.) This dose is about tenfold higher than what humans generally take -- i.e. about 0.3 mg/kg -- yet since rabbits have a faster metabolism than people relative to their size, treatments are more rapidly eliminated in that species. Regardless of this fact, the higher dose used demonstrates its safety. They found beneficial effects everywhere they looked. In the learning paradigm, galantamine made older rats perform at least as well as the younger ones. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Galantamine has dose-dependently decreased the number of trials needed to learn, demonstrating a beneficial effect even at 1 milligram per kilogram (b.w.) This treatment also shortened the action response time, a classic effect of cholinergics, and expectedly reduced acetylcholinesterase activity in the brain and plasma. [Can't see this image? Click on 'load images' or 'always allow images for this sender'] They also demonstrated an increase in epibatidine binding, a nicotine-like treatment that powerfully binds to acetylcholine receptors. This means there was either: (1) enough residual galantamine in the homogenized brain samples to exert allosteric effects, or (2) this treatment actually increased receptor synthesis just as nicotine has been shown to do (Perry, 1999). Although the experimenters had known about galantamine's APL effects at the time of publication, they chose to explain increased epibatidine binding as a consequence of receptor density.  'These findings are consistent with a report that also demonstrated a similar effect of chronic Gal therapy on nicotinic receptor density. [...] Taken together with the results of the current study, these data suggest that chronic Gal therapy can effectively and consistently increase the density of nicotinic receptors in selected brain regions that are involved in learning and memory.' ―Woodruf-Pak Either way, this is indisputably another “feather in the cap” for galantamine. Considering just how well they've been associated with cognition in general, increased brain acetylcholine receptors are a good thing no matter how they're induced. Patients with Alzheimer's disease generally have, on average, a reduced amount of nicotinic receptors compared to age-matched controls (Nordberg, 1986). This is probably why smoking has been shown preventative, and is the rationale for the use of cholinesterase inhibitors to treat the condition. 'Old rabbits treated with galantamine had the highest level of nicotinic receptor binding.' ―Woodruf-Pak As one of the few FDA-approved treatments used for this indication, galantamine has obviously not been neglected in treating dementia. However: studies show that when placed head-to-head, galantamine works at a dose lower than expected from its relative cholinesterase potency (Hansen, 2008). [Can't see this image? Click on 'load images' or 'always allow images for this sender'] Galantamine is also available over-the-counter, and undoubtedly has a better safety profile than both tacrine and rivastigmine (Hansen, 2008). So whether a person is aiming to stave-off dementia or to simply improve focus, galantamine is a safe natural compound that's worth considering. 'There is a large body of evidence to indicate that nicotinic ‘treatments’ indeed affect learning and memory. Nicotine and other nicotinic agonists can improve cognitive and psychomotor function, whereas nicotinic antagonists lead to cognitive impairment. Moreover, the incidence of AD in smokers is lower than that in non-smokers which may relate to the increased nAChR expression levels observed in the brains of smokers.' ―Maelicke 'Thus, if the therapeutic effects in AD of the three ‘treatments’ were exclusively determined by their ChE inhibitory activity, rivastigmine should be more potent than donepezil, which should be more potent than galantamine. In reality, however, this order does not apply, suggesting that, at least in the case of galantamine, a mechanism of action other than ChE inhibition must play a role.' ―Samochocki ----Important Message---- Suspicious white powder -- they stopped me at security [Can't see this image? Click on 'load images' or 'always allow images for this sender'] The TSA chaps thought this white powder was suspicious… But once I explained it to them -- that this white powder has AMAZING natural health benefits -- they were happy to let me board my plane. And now the TSA guys are all using this white powder themselves. [Here’s the “suspicious” white miracle powder that almost got me thrown off my airplane.]( ---------- Daily Medical Discoveries is dedicated to uncovering secret, buried or censored studies that can help men live great lives to 120 and beyond. You are subscribed because you joined one of our lists by opting in. We never rent or share your email address. Daily Medical Discoveries is published by Calworth Glenford LLC which also publishes other affiliated companies. By giving us your email address, you consent for Daily Medical Discoveries and its affiliated companies to delivering you a healthy daily portion of email issues and advertisements. To end your email subscription and associated external offers sent from Daily Medical Discoveries, feel free to [click here]( FREE BOOK: As a Daily Medical Discoveries subscriber in good standing, you're eligible to receive a FREE book containing underground, buried and ignored remedies that help men live a happy, healthy and sexy life to 120 years old, including specific help for men who want more sex, more life and more of everything. [Click here to claim your copy.]( Comments / Questions? You can hit REPLY to this email or email me, Matt, at matt@getrapidhelp.com Missing issues? How to make sure you NEVER miss an issue! The real key is CLICKING and OPENING emails. That shows your email provider (Yahoo, Gmail or whoever) that you WANT our email. If you don't click or open, you won't be getting them anymore, sadly. BIG TIP: Hit REPLY and say "Hi Matt" or ask a question, and THAT will assure your email provider that you want our emails! Copyright © 2021 Calworth Glenford LLC, 1005 Country Club Av., Cheyenne WY 82001 USA. Publication without written permission from Calworth Glenford is strictly prohibited. Please - you are in charge of your own life. We're not saying "don't see a doctor." We're presenting research. Don't hold us responsible if you do something as a result of what you read here. Life's all an experiment, none of us have the answers, but the more hidden/secret/censored/ignored information you have, the better off you are. We aren't doctors, and we aren't giving you personal health or sex advice! If you email us with personal information, it is our policy that we forbid our employees from sharing anything you tell us with outside parties, except if you give us permission to share it, or we are compelled by force of law to share it. Daily Medical Discoveries or its affiliated companies accept third party advertisements which will be labeled "sponsored", "third party sponsored", etc. Third party advertising helps pay the high costs of our newsletters through various business arrangements including commissions. We try to accept advertising only from legitimate advertisers, but you bear all responsibility in dealing directly with them and will not hold us responsible. Sometimes, Daily Medical Discoveries or its affiliated companies sell their own products or services and will solicit your business for those. These solicitations are NOT third party advertisements. We can stand behind anything you buy in full accord with our terms and conditions of sale, for whatever product or service you purchase.

EDM Keywords (283)

yield yet works work woman wife whoever whether whatever well weakest way want vomiting using used use us uniqueness undoubtedly try treatments treatment treat time thrown three thought think terms technically tacrine synergizes suspicious surprise suppose suggest substantial subscribed study studies strong stopped stave spared sort something solicitations solicit smoking smokers site similar shows shown share sex set services service serotonin serotonergic sender selective see security saying sale said safety safest results result responsibility responses response respectively report relation receptor receive reasons reason really read rationale rabbits question purchase published publication proven products probably primary preventing potentiating potentiate potent potency policy plasma plane person perform perfect patients order opting open one oleamide often obviously number nicotinic nicotine newsletters neglected must muscarinic mouth molecule men memory mechanism means matter matt man makes make lower looked lists list like ligands life let least learning law knows known issue involved investigate interaction instance induced indicate increasing increases increase inclusion included incidence important implies hydrolysis humans hepatotoxicity heading head happy guy grouped great go giving give getting generally general galantamine gabaa found formerly force forbid findings fact explained experimenters expected expect exhibits evidence even epibatidine enhanced end employees email eligible effectively effect doses dose donepezil doctors doctor disease discovered discontinued diazepam despite density demonstrates dementia delivering degree define deficiency dedicated daffodil counts counter could correlations convince control consistent considered consequence consent conditions compete compelled cognition clicking click class claim chose cholinergics chemists charge characterized characteristic certain central caused cause case capable cap buy business brains brain board binding beyond better belongs bearing bear average assure assuming associated ask answers amplitudes ammonia alzheimer also aiming agonist advertisements addition ad active activated action acetylcholine account 60 50 120 1000 10

Marketing emails from malehealthcures.com

View More
Sent On

22/08/2022

Sent On

22/08/2022

Sent On

21/08/2022

Sent On

21/08/2022

Sent On

20/08/2022

Sent On

20/08/2022

Email Content Statistics

Subscribe Now

Subject Line Length

Data shows that subject lines with 6 to 10 words generated 21 percent higher open rate.

Subscribe Now

Average in this category

Subscribe Now

Number of Words

The more words in the content, the more time the user will need to spend reading. Get straight to the point with catchy short phrases and interesting photos and graphics.

Subscribe Now

Average in this category

Subscribe Now

Number of Images

More images or large images might cause the email to load slower. Aim for a balance of words and images.

Subscribe Now

Average in this category

Subscribe Now

Time to Read

Longer reading time requires more attention and patience from users. Aim for short phrases and catchy keywords.

Subscribe Now

Average in this category

Subscribe Now

Predicted open rate

Subscribe Now

Spam Score

Spam score is determined by a large number of checks performed on the content of the email. For the best delivery results, it is advised to lower your spam score as much as possible.

Subscribe Now

Flesch reading score

Flesch reading score measures how complex a text is. The lower the score, the more difficult the text is to read. The Flesch readability score uses the average length of your sentences (measured by the number of words) and the average number of syllables per word in an equation to calculate the reading ease. Text with a very high Flesch reading ease score (about 100) is straightforward and easy to read, with short sentences and no words of more than two syllables. Usually, a reading ease score of 60-70 is considered acceptable/normal for web copy.

Subscribe Now

Technologies

What powers this email? Every email we receive is parsed to determine the sending ESP and any additional email technologies used.

Subscribe Now

Email Size (not include images)

Font Used

No. Font Name
Subscribe Now

Copyright © 2019–2025 SimilarMail.