The Absurdity of Pursuing Happiness

As we all know our founding fathers said that we were all created with the unalienable rights of life, liberty and the pursuit of happiness.  We are told that the purpose of government is to protect these rights.  While it makes sense that the government should protect us from being unjustly or prematurely killed and our government should protect us from being unjustly imprisoned or enslaved the government cannot do anything about our happiness.  In fact by definition no one can, not even ourselves.

The root word of the words “happy” and “happiness” is an Old English word “hap”.  The definition of the Old English word “hap” is “a chance event over which you have no control”.  Because this is the definition of “hap” when something occurs without known cause we say it just “happened.”

The word happy is used when all of your “haps” are lined up just the way you would like.  When they are you are said to be in a state of “happiness.”  But you see the problem!  If a “hap” is a chance event over which you have no control then you have no control over your “happiness.”  Happiness occurs by chance events lining up indiscriminately.  By definition no one can pursue “happiness.”

The Bible is not filled with “happy” people.  It is filled with joyful people.  “Happiness” is based on circumstances outside of oneself while joy is always found within.  Joy springs from an inner contentment based on settled belief and expectation of good.

Joy is knowing a secret.  Imagine you of one of ten students in a class.  Passing this class is a prerequisite of completing your degree and showing up and participating in each and every class is a requirement of remaining in school.  It is the day of the final exam.  No one in the class has a grade sufficient to pass the class even with a perfect score on the final exam but everyone must be present and complete the exam in order to continue in school.  Each and every student is hopeless – except you.  Last night the professor called you and admitted that the students were failing because of his failings as a teacher and that he was going to make everything right.  His plan was to give everyone in the class an A for the course on one condition.  His condition was you could not tell anyone of his plan until he did.  You had to hold in the truth.

The time for the final exam has arrived.  You are sitting in a class with nine other students who are absolutely hopeless.  As you look around the room all you see is nine empty faces, in fact anger is right under the surface.  But your fellow students notice something different on your face.  Because you know a secret and you are filled with joy, your countenance begins to rise.  In a seemingly hopeless situation you are filled with joy that you cannot contain.  Your fellow students accuse you of being crazy, not smart enough to understand the current situation.  But in fact your are the only one who knows the truth – and the truth has set you free.

The Bible is filled with people who know a secret.  It is filled with people who know who they are in Christ and where they are going.  Their circumstances are difficult but their hearts are light.  They are filled with joy!

5 Replies to “The Absurdity of Pursuing Happiness”

  1. Great post Steve.

    “felicitas” is the Latin for Happy…so even older than old English and while it does portend to a sense of happenstance…it also alludes to a sense of blessedness intricately linked to fruitfulness.

    Aquinas ties it to the natural order of things lived out. A happy dog is a dog doing and being what dogs are made to do and be (a dog with a bone). A happy man is a man doing and being what man is made to do and be.

    So how does man be what man is made to do and be? Well, it is more complex than what a dog has to figure out for sure…But I think you are right in that man is made to know things.. I don’t think that means just book knowledge, otherwise all educated people would theoretically also be happy.

    So, 1 Corinthians 13…We know in part, one day we will know in full.

    Here is how Aquinas puts it together.
    Man can experience a sort of worldly happiness (felicitas). Its actually a good and real thing. Learning skills, gaining knowledge, loving people…enjoying time with your wife for example.
    However, worldly happiness is only as good as it is realized in proportion to what it really is…temporal.

    Yet, why do we want more?
    We are finite, yet we are made for the infinite.

    So earthly happiness uh…happens, when we live how we are made to live. But even this happiness is only realized when we understand it rightly, namely that it is a shadow. Even loving some one can become inverted and distorted when we try to make them something they can never be: some sort of ultimate source of happiness. Things that make us happy are good because these natural things are good in and of themselves, (what spouse wants to be loved only and because they serve as a utilitarian signpost towards heaven). Yet they simultaneously can be received as alluding towards an even greater transcendent happiness “beatitudo” (infinite and ultimate fulfillment).

    Natural happiness (felicitas) lived with an openness towards an infinite happiness (beatitudo).
    The short hand for all that…Grace perfects nature.

    Man’s ultimate happiness (“beatitudo”) consists in pariticipation in the Divine Life (heaven). “…even as I am fully known.”

    We have it good (even when its hard) and it only gets better! I feel pretty happy thinking about that 🙂

    1. Yes, I agree whole heartedly……. Happiness is situational or circumstantial. It is an emotion of the flesh that can come and go. Things, people, etc. can make us happy. But Joy is spiritual; it is from a true relationship with God. It is forever! We can be unhappy, sad, or mournful, but still have joy. Thank you Jesus. Praise be to God!

  2. Due To This Fact, inhibition of Wnt signaling downregulated MSC
    proliferation (Steelman et al., 2006). Altogether, these findings
    recommend the complexity of MSTN signal transduction might be due
    to the involvement of different signaling pathways and that the precise integration of those
    pathways underlies the expansion inhibitory results of MSTN.
    In addition, we also review the state-of-the-art in silico approaches used to
    design MSTN inhibitors primarily based on the constructions of its interacting proteins.

    A myostatin inhibitor prevents myostatin from binding
    to its receptor, thereby repressing the downstream Smad-pathway [11].
    By supplementing it, you can experience benefits in muscle growth and power and enhancements in vascularity,
    blood flow, and endurance. Training with heavy weight doubtless provides a suggestions
    stimulus that inhibits myostatin, partially to allow for useful muscle progress processes to kick in.
    If this didn’t occur, we might return to the
    gym time and again with minimal gains to show for it.
    Coupled with the myostatin inhibition that resistance training itself elicits,
    there could also be no room for one more inhibitor to work.
    The examine concludes that additional tests are needed to see
    whether or not creatine, leucine and HMB are synergistic with respect to
    myostatin inhibition (and other growth pathways) or not.

    Consequently, it’s unlikely that the positive results of increased protein or
    power intake might be achieved without controlling these factors [14].
    Additionally, hormonal medications could depart various adverse results,
    like androgens which will trigger virilism and/or worsening of atherosclerosis [133].
    The synthetic androgenic agent nandrolone and the
    human development hormone (GH) can enhance lean body mass.
    Nevertheless, using human GH is expensive, and solely male sufferers
    could benefit from nandrolone [134]. Conversely, different drugs
    including antioxidant/anti-inflammatory agents and urge for food stimulants could be efficient and promising.
    C2C12 cells had been also cultured in a myogenic differentiation medium supplemented with Ac-MIF1 or Ac-MIF2-NH2 for three days.

    The majority of those approaches acts extracellularly to dam myostatin partaking with
    the ActRIIB/Alk4/5 receptor complicated, both by binding directly to
    myostatin itself or by binding to parts of this
    receptor complex. Equally, the naturally occurring myostatin binding proteins follistatin and Fstl3 are known to
    bind numerous development factors along with myostatin [28,29].
    The added risk/benefit of those multitargeted approaches is underneath investigation (see below).
    The influence of various dietary lipids on the metabolism of muscles and
    the regulation of E3 enzymes has been assessed in a number of investigations; however, none have targeted on CKD.
    Scientific studies have indicated the upregulation of the
    NRF2 gene following administration of omega-3 (2700 mg/day) in diabetic individuals, attributed to the antioxidant effects of NRF2
    [186].
    Lastly, experiment with the epicatechin dosage that appears to greatest suit your wants.
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    A case study of a human youngster with unusually excessive levels of muscle
    growth reported that the child additionally had very low ranges of myostatin.
    The authors instructed that myostatin inhibition might have been involved within the noticed enhanced
    muscle development, though no other related instances have been reported [18].
    First, some evidence suggests that inhibiting myostatin can stop muscle from weakening throughout lengthy
    intervals of inactivity. For example, myostatin inhibition lowered the loss
    of muscle in young mice that have been prevented
    from using their hind legs for 21 days [11].
    Myostatin is a cytokine that works by inhibiting the proliferation of satellite tv for pc
    cells and the differentiation of myoblasts [10], while additionally lowering
    adipogenesis by way of reductions in the secretion of leptin [11].
    Thus, the rationale for binding myostatin with sulfo-polysaccharides would theoretically result
    in elevated muscle mass and improved physique composition. The curiosity in myostatin was generated by current research the place antibodies
    for myostatin were created and administered to grownup rodents, which resulted in a rise in physique mass, muscle mass, muscle size, and energy [11,12].
    Despite the success in rodents, human fashions have not
    been as successful in increasing body mass and muscle mass [13], but sulfo-polysaccharides have been reported to have a binding specificity for
    the myostatin inhibitor follistatin [14].
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    The specificity of the PCR was demonstrated with an absolute negative control reaction containing
    no cDNA template, and a single gene product was confirmed utilizing DNA melt curve evaluation. YK11 is a SARM that
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    Bodybuilders who rely on muscle development supplements have switched to YK11 as a result of they imagine it’s safer
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    The pro-domain incorporates N-terminal “forearm” helices, which grasp mature GF, and a globular “arm/shoulder” domain, which sits on prime of the mature GF protomers (Cotton et al.,
    2018). Each MSTN monomer has 4 intermolecular disulfide bonds,
    three of that are concerned in cysteine knot formation. When the 2 monomers of MSTN come together in an antiparallel course they generate convex or concave
    surfaces. Nonetheless, later x-ray structural analysis demonstrated
    that it is a member of the TGF-β superfamily, though it reveals exceptional differences in the N-terminal
    region and within the region previous the wrist helix (Cotton et al.,
    2018). GH-mediated conversion of thyroid hormone (TH) thyroxine (T4) to triiodothyronine (T3) helps their distribution to different tissues
    through binding to thyroxine-binding globulin,
    albumin, or transthyretin (TTR) (Alshehri et al., 2015).
    TTR-based T4 distribution was found to promote myoblast differentiation by regulating the expressions of myosin light chain 2
    (MYL2) and the calcium channel genes Cav1.1 and Cav3.1 (Lee et al., 2013).
    We lately reported that in myoblast differentiation, TTR maintains muscle homeostasis via the unique
    TH shuttle mechanism.
    In the present examine, remedy of myotubes with 50 µM UA elicited
    a 21% improve in basal glucose uptake, which was preserved however not further enhanced within the
    insulin-stimulated state. This suggests that UA has comparable potential to confer
    helpful effects in skeletal muscle glucose uptake in each the post-absorptive and post-prandial state.
    While GLUT4 abundance in major human myotubes is
    low, it is still significantly recruited to the plasma membrane
    upon insulin stimulation [33] and is translocated in C2C12 cells upon stimulation with
    low doses of EA [34]. This observation due to this fact warrants additional
    investigation under in vivo conditions. Have you tried every little thing possible to develop more muscle and nothing seems to work for you?

    In Addition To, PLA leads to the development of the aberrant molecular signaling pathways associated to muscle losing
    in CKD (i.e. proteolysis, myogenesis, and muscle regeneration,
    and the expression of pro-inflammatory muscle cytokines) [147].

    The results of an animal uremic cachexia and renal fibrosis model confirmed that PLA might be a dependable therapy for CKD-related cachexia,
    muscle, and kidney fibrosis to enhance the standard of life and survival of
    CKD circumstances [148]. Myostatin, a member of the
    reworking growth issue beta (TGF-β) superfamily, was first described in 1997.
    Since then, myostatin has gained rising consideration because of the invention that myostatin inhibition results in muscle mass accrual.

    Myostatin not only plays a key position in muscle homeostasis, but also affects fat and bone.

    This good little study truly highlights the already well documented body of proof that’s led many scientists and specialists to
    imagine creatine is anabolic whereas Leucine
    and HMB are anti-catabolic. Properly, that’s finest answered by
    talking concerning the other three supplements, I talked about earlier on this article.
    It’s been discontinued now, however MYO-X is probably the bodybuilding world’s most well-known patented myostatin inhibitor.
    So, scientists have identified tips on how to inhibit myostatin in animal research for a really long time
    now and they’ve experimented with alternative ways of doing
    it, and at different phases within the life-cycle.
    The information on this web site has not been evaluated by the Meals & Drug
    Administration or any other medical physique. You must consult your doctor before
    appearing on any content material on this web site, especially if you are pregnant, nursing, taking medication, or have a
    medical situation. The opinions expressed in this part are solely these of the customers who may or may not have medical
    or scientific training.
    Adjustments in accessible floor space (ASA) confirmed
    the residues in this region of MSTN exhibited most ASA modifications after binding with FMOD or ACVRIIB.
    Statements concerning supplement benefits have not been evaluated by the Food and Drug Administration. Clear Labs merchandise
    aren’t intended to diagnose, treat, cure, or forestall any disease.

    Throughout this session, each participant performed a
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    Change in serum lively testosterone levels (mean ± SD) between teams following eight weeks of resistance training and supplementation.
    Change in serum free testosterone ranges (mean ± SD) between groups
    following eight weeks of resistance training and supplementation. Subjects participated in a
    periodized 4-day per week resistance-training program split into two
    higher and two lower extremity exercises per week
    for a total of 8-weeks. Prior to the exercise, topics carried
    out a standardized sequence of stretching workout routines
    as a warm-up. Topics then carried out an upper physique resistance-training
    program consisting of 9 workouts (bench press, lat pull, shoulder press, seated rows,
    shoulder shrugs, chest flys, biceps curl, triceps press down, and stomach curls) twice
    per week. Topics also carried out a seven-exercise decrease extremity resistance-training program that might embody (leg press, squat, back extension, step-ups,
    leg curls, leg extension, heel raises, and stomach crunches) twice per week.

    An fascinating discovering in a number of the analysis is that sure myostatin inhibitors would possibly assist with
    muscle development, but energy and performance are probably weakened, relative to dimension.
    These findings make me think myostatin expression hasn’t necessarily evolved to be a
    adverse growth factor to all kinds of muscle hypertrophy pathways.
    If it had, then it would make no sense that resistance training inhibits myostatin.
    By pooling research on the subject, that report (which is also
    pretty latest, from 2014) tells us that more studies have found
    myostatin inhibition to help with muscle function/strength enhancements in addition to the increases in mass.
    Muscle protein synthesis is the method of building proteins which is able to ultimately make up the protein content material of muscle fibers.
    Myostatin is a natural protein active in a quantity
    of species of animal, together with us humans.
    MicroRNAs are a class of small non-coding RNAs that play a significant role in regulating muscle metabolism,
    growth, renewal, and degeneration [114]. Latest
    analysis has established that miRNAs play a job within the management of CKD-triggered
    muscle loss by enhancing protein breakdown or hindering myogenesis.
    Muscle loss in the setting of CKD correlates with a discount in miR-26a,
    whereas an elevated level of miR-26a mitigates CKD-triggered muscular atrophy through blocking the FOXO1 transcription factor [31, 115].
    A reduction in miR-29 levels results in the rise of YY1 transcription element perform, therefore impeding myogenesis, whereas an elevated degree
    of miR-29 mitigates CKD-triggered losing of muscles through downregulating TGF-β, and YY1 axis proteins [116, 117].

    It is a monoclonal antibody with an IgG4 Fc domain designed for sarcopenia and inclusion body myositis
    (IBM) treatment. Trevogrumab targets MSTN in its
    mature, latent, and pro-forms with out cross-reactive binding to GDF11 [57].
    Apitegromab, developed by Scholar Rock, particularly targets MSTN
    in its latent kind by stabilizing its conformation, thereby preventing access to prodomain protease
    cleavage sites [58, 59]. Apitegromab has shown efficacy in growing muscle mass
    and performance in mouse fashions of spinal muscular atrophy
    (SMA) [60].
    Expression of those genes has been linked
    to larger atrophy of fast-twitch fibers in limb immobilization51, which we also
    observed. Nonetheless, elevated catabolic processes weren’t accompanied by lowered Akt activation in contrast to other research where Akt ranges
    were lower at 7 and 14 days of HS9,52. Biomarkers of protein synthesis were not considerably completely different, despite the very fact that p70S6K phosphorylation elevated early in HS53 followed by reduced activation at 7 days52.

    Future work evaluating downstream targets of p70s6k would
    be particularly informative. Taken together, these outcomes suggest that at our research endpoint following two weeks of HS, muscle atrophy
    resulted from larger protein degradation somewhat than reduced protein synthesis9.
    Regardless Of yielding positive leads to numerous animal studies, MSTN
    inhibition has not improved human muscular operate.
    This study examined 12-weeks of resistance coaching and cystoseira
    canariensis supplementation on serum ranges of myostatin and muscle
    strength and body composition in twenty-two untrained males.
    Training consisted of three days per week using three units of 6 to 8 repetitions at 85–90% 1
    RM. The researchers concluded that 12-weeks of heavy
    resistance coaching and 1200 mg/d of cystoseira canariensis supplementation seemed to
    be ineffective at inhibiting serum myostatin and rising muscle energy and mass or decreasing fat mass.
    The clarification for the dramatic effects in animals while no observed
    results in people in all probability lies in the truth that myostatin particular
    antibodies had been used within the animal model, whereas human models use sulfo-polysaccharides that are only marketed to bind to myostatin. Results of this examine assist this prior report in that
    CSP3 supplementation had no important effects on body
    composition, training variations, or markers of anabolic/catabolic standing in resistance-trained males.

    Ever since its discovery, intensive research has been conducted to
    suppress the activity of MSTN utilizing soluble activin type IIB (sACVRIIB) receptors, peptides or
    propeptides, small molecules, neutralizing
    antibodies, or MIPs (Table 1). Based in Canada, Katrina is an experienced content writer and editor specializing in well being and wellness.
    With a journalistic strategy, she’s crafted over 900,000 words on supplements, striving to
    debunk myths and foster a holistic approach to healthi…

    Although epicatechin and quercetin are considered safe supplements, don’t go all in without doing
    your individual research. If you are on medications or have
    a health condition, this means talking with your healthcare skilled
    to ensure it’s applicable for your health objectives.
    By doing this, you can also make more informed decisions,
    maximizing your efforts whereas safeguarding your well being.

    Inhibiting MSTN might have therapeutic applications in selling bone regeneration and therapeutic in bone fractures, osteoporosis, rheumatoid
    arthritis, and osteoarthritis. In mice, administration of recombinant MSTN propeptide improved
    fracture therapeutic in a fibula osteotomy mannequin [150].
    Additionally, treatment of younger mice with ActRIIB-Fc led to elevated bone mass
    [151].

    References:

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