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Call to Action | VEPA

A key part of any sales pitch, be it on the Web or otherwise, is the call-to-action. A call-to-action is a group of words which encourages a reader, listener, or viewer of a website to enact on a desired response. A desired response is simply the next desired action you would like from a prospective customer (i.e. making a purchase, signing up for a newsletter, etc.). Therefore an advertisement or commercial without a call-to-action is considered incomplete and ineffective.

The acronym VEPA is often used when entrepreneurs talk about calls-to-action. VEPA stands for:

V = Value: The customer should get some value out of the desired action

E = Ease of use: The desired action should be easy for the customer to execute

P = Prominent: The action should be prominent and easy to see

A = Action: The wording should speak to action (ex. Buy Now!)

You should continually play with VEPA and your calls-to-action to maximize desired responses from customers. There are various effective online tools to help you multivariate test your calls-to-action. One of the most powerful free options is Google’s Experiments. You can play with and test various attributes such as bigger or different color calls, changing the calls’ copy, or different incentives for customers to act upon. Incentives can go a long way if done correctly.

An effective call-to-action is the linchpin of a successful sales campaign and involves drawing together best practices in usability, creativity and effective but concise copy writing. It all starts with a great call-to-action button, here are 25 examples of call-to-action buttons to get your creative juices flowing.

Three Types of Certainty

Peak performers live their life with a high degree of certainty that they can achieve their goals. There are three different types of certainty: 1) opinion; 2) belief; and 3) conviction. Opinions are formed through transitory perceptions and it is easy to reformulate opinions based on new information and inputs. The fleeting nature of opinions make them a bit precarious as a useful tool for achieving goals. For instance, going out for a long run with just an opinion of successfully completing the run, you can easily be sabotaged to a new opinion of inadequacy when you begin to feel fatigued and/or feel like quitting.

Our beliefs are much stronger. Beliefs are often attached to emotional occurrences (ex. not wanting to be overweight) and/or reoccurring events (ex. habitual exercise) which create stronger neural pathways in the brain (than opinions). It is possible to change our beliefs as well but it requires more effort than merely changing an opinion about something. Using the same running analogy, a belief can help you push through fatigue because personal experience and prior accomplishments create resolve.

The highest form of certainty is our convictions. Throughout history many have achieved incredible successes through conviction, where others have created incredible chaos. Using the running analogy, a runner with a conviction to finish might push through an injury to complete a race (at considerable risk).

Convictions are extremely empowering (for better or worse) and can operate indiscriminately of ethical boundaries and common sense. There is much debate in psychology about the formation of convictions. Classic nurture versus nature arguments are applied throughout broad topics ranging from religious convictions to prejudicial ideologies. The truth is there’s still a lot we don’t know about how people develop their concepts of certainty.

What we do know is that certainty is needed to help drive decisions and initiate tasks. This should be intuitive… if someone can’t make up their mind this indecisiveness usually leads to inaction, and a lack of action is the quickest way to get nowhere. Peak performers create positive certainty by creating experiences and references that strengthen their beliefs and convictions. In the beginning this can be as simple as gathering information and talking to people that have previous knowledge. Eventually it requires taking continuous action. Action advantageously strengthens certainty and moves opinions to beliefs, and beliefs to convictions, which of course leads to more positive action. This loop creates powerful cycles that lead to continuous improvement.

There are risks and costs to action. But they are far less than the long range risks of comfortable inaction.
— John F. Kennedy

The Volumetrics Diet

Most of the popular diets today rely somewhat on portion control. However, one diet offers an alternative. The diet method is called Volumetrics and the premise is to encourage people to eat foods that are naturally low in calories due to high water content. Fresh produce, whole grains, good fats and low-fat dairy are all available food choices on the Volumetrics diet.

The benefit of Volumetrics is that one can potentially lose weight without decreasing their food portions. This can help eliminate the feeling of hunger that accompanies certain types of diets. The premise is that a full stomach will limit feelings of hunger and make the regimen feel less like a diet than other alternatives potentially leading to adherence.

Accordingly the primary focus of this diet is changing one’s food choices as opposed to meal reduction. For example, calorie dense foods like butter, cookies, oil and candy are to be substituted with foods that have fewer calories by mass and volume. However, that doesn’t mean you can’t still indulge in old favorites. For instance, macaroni and cheese can be made healthier by replacing the usual ingredients with whole-wheat pasta, no-fat milk, low-fat cheese and margarine. Food preparation is also optimized in this dietary plan through boiling and grilling as opposed to any type of cooking that requires oil.

Because the body stays hydrated during the Volumetrics diet it probably won’t appeal to those looking to shed quick pounds through the diuretic effect of low carbohydrate diets. Don’t expect to lose more than two pounds a week on this diet. It is not a quick fix. Like any diet your results will depend on obedience to the plan and maintaining an exercise regimen. However it might be just what you are looking for if you are opposed to reducing portion size but are willing to make different food choices.

A great cookbook on the subject is available from the best-selling author and nutrition professor Dr. Barbara Rolls entitled The Volumetrics Eating Plan: Techniques and Recipes for Feeling Full on Fewer Calories (if Volumetrics is not your thing you can see more healthy cookbooks by clicking here). If you have had any luck (good or bad) with Volumetrics please let me know in the comments section below.

Great Entrepreneurial Ideas Get Help | The Penny Ice Creamery

Recently I attended a meeting with my local chamber of commerce and was made aware of the story behind a neat little start-up, The Penny Ice Creamery. The Penny Ice Creamery is an artisan ice creamery located in Santa Cruz, California, that successfully used government programs to get their business flourishing. They are a “real world” example of what a great business plan along with thoughtful execution can achieve.

The video above shows how The Penny Ice Creamery was able to maneuver their way through the American Recovery and Reinvestment Act enabling business partners Kendra Baker and Zach Davis to successfully deploy their entrepreneurial vision. It also illustrates the value that small business plays in a community by highlighting job creation and purchasing from local and national suppliers. If nothing else it is a testament to what can be achieved with fortitude and another example that great entrepreneurial ideas get help when needed.

10 Tips to Increase Self-Control

Another consistent trait of peak performers is their high aptitude for self-control. Self-control is our ability to stay steadfast regarding long-term goals despite natural human urges to partake in activities that are instantly gratifying. In excess, instantly gratifying activities can often lead to various forms of destructive addiction. Many instantly gratifying activities also lack the positive compounding effects that activities with deferred gratification possess. Many of you probably remember the Stanford Marshmallow Experiment on this subject. Here is a great little video highlighting how easy it is to be tempted, even when promised a greater reward in the future.

Training and acquiring mastery in anything requires work and practice. The good news is that there are many ways we can train ourselves to improve self-control. Here are 10 tips to increase self-control from the May / June 2011 edition of Scientific American Mind:

  1. Become aware of the risks and long term negative consequences of undesirable behavior.
  2. Increase your personal engagement by, for example, telling friends about your goals.
  3. Transform abstract overarching objectives into intermediate steps or milestones.
  4. Take pleasure in achieving partial successes and reaching intermediate milestones.
  5. Formulate “if then” resolutions to deal with critical situations.
  6. Replace old bad habits with new good ones.
  7. Change your impulse by learning to associate the mere sight of temptations with negative stimuli.
  8. Identify situations that pose a particular risk and avoid them as much as possible.
  9. Train you working memory.
  10. Plan enough breaks and relaxation periods to prevent depletion of your mental resources.

If you have any additional tips on how to increase self-control please share them in the comments section below.

When should I replace my running shoes?

When should I replace my running shoes? Finding the right running shoe is an iterative process and there is no one perfect running shoe suitable for everyone. The perfect fit has to do with the shape of your foot, your running style and the terrain you run on. In fact, there are runners who don’t seem to need shoes at all. Many endurance sport injuries are purportedly caused by using worn out shoes, and there are many factors which help a runner determine whether it is time for a change of shoes.

When should I replace my running shoes?

One important factor is mileage – one school of thought is to replace running shoes every 250 miles, where others recommend changing shoes after running 300-500 miles. So how should a runner gauge his mileage? This is where your training log comes in. Documenting your effort is the best gauge on getting a true sense of what is right for you.

Time is another factor – a generally accepted duration is 6 months. This has been calculated by assuming a regular weekly schedule of 3 to 5 mile runs / 4 days a week. A runner who follows that schedule would change shoes around the 300-500 mileage mark. Logically, a runner who runs more miles would find it necessary to replace his/her shoe earlier than the general 6-month rule.

Other important factors include weight and running style. Clydesdale/Athena runners (like myself) might find themselves changing shoes more often as carrying extra weight can break down shoes faster. Lightweight runners who are heavy footed or use unique running techniques will also burn through shoes quicker.

How can you tell if your shoes are showing signs of wear? Place your shoes at eyesight level and look at the back of your shoes. If the soles look worn out and appear uneven, there could be some damage to the midsole. The midsole is one of the more important parts of the shoe. However, finding a defect is not easy. If you feel tightness, fatigue, aches and pains while running, then it can be an indication of midsole damage. Try twisting your shoe, if it twists easily then it might have a damaged insole. Similarly you can check the other parts of the shoe — wear can affect the cushioning, back heel, arch point or the toe box of the shoe as well.

Knowing the condition of your shoes is important because neglecting their condition may lead to injury. A tip for longer shoe life, try rotating shoes during a training week. Not only will it reduce mileage on each pair, it is a great way to test different brands to determine which shoe is giving you the best performance.

Finding the right running shoe is not an exact science, it depends on the various factors I have mentioned above (plus more). You are the best person to determine what works. Log your training and keep notes about how you feel, plus how your shoes feel, and you will quickly be able to answer the question, “When should I replace my running shoes?” for yourself.

Can mitochondria generated during mitochondriogenesis create free radicals?

The shortest answer is no. Consider a given mass of tissue. If for that tissue, we ask what is the most rate limiting – the number of mitochondria or substrate and oxygen utilization? The best answer is usually substrate and oxygen. For typical activities we have plenty of mitochondria and with normal rates of substrate utilization and hydrogen transfer, oxygen is efficiently converted to water. However, if substrates are: 1) limiting (i.e. from carbohydrates, lipids, or proteins/amino acids) as might be the case at the end of a long intense exercise, 2) or areas of tissue damage, wherein substrates might be used inappropriately used, 3) or aging, wherein the metabolic machinery incased in mitochondria is decreased – there is less potential for oxygen to be effectively converted to water. ROS (reactive oxidant species) may be generated to make the situation worst. Optimizing mitochondrial amount does not necessarily generate more ROS (except in situations where oxygen flux through the metabolic pathways in mitochondria is very rapid and/or is not efficiently utilized. This may happen during the course of running a marathon or sprinting, where relative to oxygen, the metabolic substrates used as fuel sources are limited. It can also happen when electron transport inhibitors uncouple electron transfer to oxygen. However, regarding each of these examples, a case may be made that recovery is better and faster when substrate utilization and oxygen become more in synch and when all of the mitochondrial machinery is functional and optimized. In areas of tissue damage, having more or optimizing mitochondrial function is consistently reported to lessen tissue damage due to ROS. There are now dozens of papers that support the notion that retarding aging is a direct function of optimizing mitochondrial function.

Regarding your other comments, we prefer not to think of PQQ as a vitamin. The claim was made, because of misinterpretation of the original data used in support of that notion. Rather, pyrroloquinoline quinone is best categorized as one of several compounds that act as cell signaling molecules. It is also not clear how “massive” a dose of 10-20 mg PQQ per day actually is. The assays used to date in various studies have measured only PQQ. It is known that in human milk, about 80-90% of the PQQ is in derivation form (products derived from PQQ reacting with amino acids). Some of these derivatives have effects similar to PQQ in studies in vitro.

Is there a vitamin PQQ should be taken with?

Are there any other vitamin supplements that work well with PQQ?

As you are probably aware from reading PQQ, pyrroloquinoline quinone seems to act in promoting mitochondriogenesis and, in a broader context, by protecting neural tissue. Compounds that may promote mitochondriogenesis included resveratrol, quercetin, and hydroxytyrosol (found in olive oil). Other agents that promote mitochondrial function and performance may be synergistic. Such compounds include CoQ10 and carnitine. They either facilitate various metabolic events or aid in moving substrate into and out of the mitochondria. The point here is that just because both PQQ and CoQ10 are quinones, they are doing very different things. One would not want to substitute one for the other. Also, consider the following, consuming a traditionally well-balanced diet (with or without supplements) and regular aggressive exercise is also an excellent formula to stimulate mitochondriogenesis, particularly in muscle. Think of given supplements as a way to potentially optimize this process.

Does lipoic acid function synergistically with PQQ, vitamin C or other antioxidants?

Lipoic acid is a cofactor for one of the first steps in a major mitochondrial metabolic pathway. Ascorbic acid plays a number of cellular roles – only a few are specific to mitochondria. As chemicals, they work quite differently in the human body. There are a number of references that one can cite. The following is a good example. (Valdecantos et al. Vitamin C, resveratrol and lipoic acid actions on isolated rat liver mitochondria: all antioxidants but different. Redox Rep. 2010; 15:207-16).

What are some good antioxidants?

Many compounds are touted as better or worst regarding there antioxidant potential in chemical assays. In a recent paper, leaders in this field have pointed out that for many types of antioxidants, there effects are due to mechanisms that have little to do with their antioxidant potential (e.g., Hollman et al. The Biological Relevance of Direct Antioxidant Effects of Polyphenols for Cardiovascular Health in Humans Is Not Established. J Nutr. 2011 Mar 30). Although some compounds exert beneficial effects on some biomarkers of cardiovascular health, there is no evidence that this is caused by improvements in their antioxidant capacity. Rather, the real mechanisms have to do with cellular signaling, or the up- or down-regulation of complex metabolic pathways. To use, PQQ as an example, in chemical assays, it is easy to set conditions so that it may function as both a potent pro- and anti-oxidant. What pyrroloquinoline quinone can potentially do is stimulate mitochondriogenesis. The best way a cell has to coordinate oxidative and free radical potential is to optimize cellular organelles, such as mitochondria that are directly involved in oxidative metabolism.

PQQ, glutamate, nitric oxide and N-methyl-D-aspartic acid receptors

What are the effects of pyrroloquinoline quinone on glutamate? And, can PQQ be used for neuroprotection?

Some of the earliest reports regarding the potential physiological functions of PQQ have involved studies focusing on PQQ and neural function and neuroprotection.  In experimental animal models, the effects of pyrroloquinoline quinone on glutamate are mechanisms that protect the redox modulatory site of so-called “glutamate receptors”. Glutamate receptors are located primarily on the membranes of neuronal cells. This class of receptors is responsible for glutamate-mediated excitation of neural cells that are important for neural communication, memory formation, learning, and regulation.

Glutamate is the most prominent neurotransmitter in the body.  The common name for the two primary glutamate receptors actually derives from the chemical names of two agonists used to study them, i.e., the AMPA receptor that binds to both glutamate and α-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate (AMPA) and the NMDA receptor that binds to both glutamate and N-methyl-D-aspartate or NMDA.  An agonist is a chemical that binds to a receptor of a cell and triggers a response in a cell similar to that of the native or more physiological receptor.

In many of the studies, the N-methyl-D-aspartic acid (NMDA) receptor has received the most attention.  It is a specific type of glutamate receptor involved in ion-transport. Agents that protect NMDA-receptor function are often neuroprotective. With regard to PQQ, exposure to PQQ either in vitro or in vivo has been shown to promote the recovery of from spinal cord injury in rats after hemi-transection (Hirakawa et al. Biochem Biophys Res Commun. 2009; 378:308-12) and counteract the effects of potent neurotoxins, such as 6-hydroxydopamine (Hara et al. Neurochem Res. 2007; 32:489-95).  A number of studies have also shown that PQQ can act as a neuroprotectant in animal models of stroke therapy and ischemic stroke (Zhang et al. Brain Res. 2006; 1094:200-206; Zhang et al. Eur J Neurosci. 2002; 16:1015-1024; Aizenman et al. J Neurosci. 1992; 12:2362-9; Jensen et al. Neuroscience. 1994; 62:399-406; Scanlon et al. Eur J Pharmacol. 1997; 326:67-74). A very interesting feature relates to the promotion of nerve regeneration of transected nerves when tissue damage/repair is involved (Li et al. Chin J Traumatol. 2005; 8:225-229; Lui et al. Microsurgery 2005; 25:329-337). When one couples this in formation to that which indicates PQQ and some of its derivatives can stimulate nerve growth factor synthesis, it indicates a very promising potential for the use PQQ in correcting damage to neural tissue (Murase et al. Biosci Biotechnol Biochem. 1993; 57:1231-1233; Urakami et al. Biofactors. 1995-1996; 5:139-146).

Neurological manifestations caused by neural injury may also be influenced by PQQ.  For example, protection of the NMDA receptor redox modulatory site by PQQ has been shown to improve the pathophysiology of seizures. Rat pups with chemically induced convulsions and seizures are protected by PQQ administration (Sanchez et al. J Neurosci. 2000; 20:2409-2417).  All of these observations are promising, although a direct link to human disease needs to be made.  All of the studies to date have utilized rodent models.

How is neuronal protection achieved?

With regard to damaged nerve fibers, several studies suggest PQQ can protect against secondary damage by reducing the expression or production of the enzyme, nitric oxide syntheses (NOS), following a primary physical injury to the nerve.  NOS enzyme activity and its major product are essential to nerve function. Low levels of nitric oxide production, the product from an NOS reaction, are important in protecting an organ from oxidant damage.  However, one can also relate its activity to nerve damage in the following way.  First, similar to other tissues, following injury or damage, increased amounts of reactive oxygen species (ROS) are often produced.  Some of these ROS products can react with nitric oxide to form peroxynitrite as an additional potential by-product. Although nitric oxide (produced by the action of NOS) is an important cellular signaling molecule, its product, peroxynitrite, resulting from the reaction of NO with ROS is a compound with potent damaging oxidant potential. Thus, the demonstration that inducible NOS expression and peroxynitrite formation is depressed or decreased by PQQ is one potential mechanism for PQQ’s action (Zhang & Rosenberg. Eur J Neurosci. 2002; 16:1015-24; Hirakawa et al. Biochem Biophys Res Commun. 2009; 378:308-12).

Moreover, PQQ’s ability to influence the levels of the cell signaling molecule, DJ-1, adds an additional dimension. DJ-1 is a neuronal cell-signaling molecule and plays a role in oxidative stress reactions important to optimizing neurological function and protecting against inappropriate cell death. DJ-1 has also been shown to be the same protein as PARK7 (Parkinson disease autosomal recessive, early onset 7), which has been implicated in early onset Parkinson’s disease.   PQQ increases the level of an active form of DJ-1 (Nunome et al. Biol Pharm Bull. 2008; 31:1321-6).  As this information develops as well as that related to the effects of PQQ on other signaling molecules, it should soon be possible to extract a precise mechanism of action.  For example, it has recently been shown that the glutamate-induced apoptosis (early cell death) in cultured neurons is significantly reversed by PQQ treatment.  In addition, examination of several key cell-signaling molecules, which work in tandem with components of the glutamate receptor signaling pathways, has revealed that PQQ treatment stimulates their activation (Zhang et al. Toxicol Appl Pharmacol. 2011; 252:62-72).

What does mean to the consumer of supplements?

First, as pointed out in our other discussions. A compound may be a good “chemical” antioxidant in assays in vitro, but do little to improve a pathophysiological condition in vivo.  Cellular antioxidant activity is mostly controlled by the regulation of metabolic processes (mostly enzymes) that in turn are highly regulated by events that take place in complex and interactive cell signaling pathways.  PQQ is know now known to influence a number of these pathways neuronal cells at relatively low levels of intake.   Whether PQQ has any clinical efficacy in the treatment of stroke, Parkinson’s disease, or any of the mitochondrial-related neurological diseases remains to be seen.  However, many investigators are excited about the potential of this prospect given the positive responses to PQQ in experimental models of neurological disease.